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1. Biomedical articles (top 50; 2009 to 2014)
1. |||||||||. 100%  Cooper IF, Siadaty MS: 'Amino Acids, Peptides, or Proteins' associated with 'Brain Hypertrophy': Top Publications. BioMedLib Review; AminoAcidPeptide;BrainHypertrophy:705745795. ISSN: 2331-5717. 2014/4/26
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  • [Title] 'Amino Acids, Peptides, or Proteins' associated with 'Brain Hypertrophy': Top Publications.
  • Background: There are articles published each month which present 'amino acid peptide or protein' for 'brain hypertrophy'.
  • Takahashi N et al: Angiotensin II-induced ventricular hypertrophy and extracellular signal-regulated kinase activation are suppressed in mice overexpressing brain natriuretic peptide in circulation.
  • Liang F et al: Triiodothyronine increases brain natriuretic peptide (BNP) gene transcription and amplifies endothelin-dependent BNP gene transcription and hypertrophy in neonatal rat ventricular myocytes.
  • Saliba Y et al: Microalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats.
  • Baltatu O et al: The brain renin-angiotensin system modulates angiotensin II-induced hypertension and cardiac hypertrophy.
  • Ando H et al: Angiotensin II AT1 receptor blockade reverses pathological hypertrophy and inflammation in brain microvessels of spontaneously hypertensive rats.
  • Kohno M et al: Effect of angiotensin-converting enzyme inhibitor on left ventricular parameters and circulating brain natriuretic peptide in elderly hypertensives with left venticular hypertrophy.
  • Murakami Y et al: New insights into the mechanism of the elevation of plasma brain natriuretic polypeptide levels in patients with left ventricular hypertrophy.
  • Katz E et al: T4-induced cardiac hypertrophy disrupts cyclic GMP mediated responses to brain natriuretic peptide in rabbit myocardium.
  • Rogers RK et al: Diagnosis and characterization of left ventricular hypertrophy by computerized acoustic cardiography, brain natriuretic peptide, and electrocardiography.
  • Luchner A et al: Evaluation of brain natriuretic peptide as marker of left ventricular dysfunction and hypertrophy in the population.

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 705745795.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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2. |......... 4%  Basir R, Rahiman SF, Hasballah K, Chong W, Talib H, Yam M, Jabbarzare M, Tie T, Othman F, Moklas M, Abdullah W, Ahmad Z: Plasmodium berghei ANKA Infection in ICR Mice as a Model of Cerebral Malaria. Iran J Parasitol; 2012;7(4):62-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Histopathological findings revealed several important features mimicking human CM including, microvascular sequestration of PRBCs in major organs, particularly in the brain, hypertrophy and hyperplasia of the kupffer cells in the liver, pulmonary edema and hyaline membrane formation in the lungs and haemorrhages in the kidney's medulla and cortex.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 23323093.001).
  • [ISSN] 1735-7020
  • [Journal-full-title] Iranian journal of parasitology
  • [ISO-abbreviation] Iran J Parasitol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Other-IDs] NLM/ PMC3537477
  • [Keywords] NOTNLM ; Animal model / ICR mice / Malaria / Plasmodium berghei
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3. |......... 4%  Moreno H, Burghardt NS, Vela-Duarte D, Masciotti J, Hua F, Fenton AA, Schwaller B, Small SA: The absence of the calcium-buffering protein calbindin is associated with faster age-related decline in hippocampal metabolism. Hippocampus; 2012 May;22(5):1107-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although reductions in the expression of the calcium-buffering proteins calbindin D-28K (CB) and parvalbumin (PV) have been observed in the aging brain, it is unknown whether these changes contribute to age-related hippocampal dysfunction.
  • We also found age-independent structural changes in CBKO mice, which included an enlarged hippocampus and neocortex as well as global brain hypertrophy.

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  • [Copyright] Copyright © 2011 Wiley Periodicals, Inc.
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  • (PMID = 21630373.001).
  • [ISSN] 1098-1063
  • [Journal-full-title] Hippocampus
  • [ISO-abbreviation] Hippocampus
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG025161; United States / NIA NIH HHS / AG / AG027476; United States / NIA NIH HHS / AG / AG034618; United States / NIA NIH HHS / AG / K08 AG027476-05; United States / NIA NIH HHS / AG / K23 AG000946; United States / NIA NIH HHS / AG / P50 AG008702; United States / NIA NIH HHS / AG / R01 AG025161
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calbindins; 0 / Parvalbumins; 0 / S100 Calcium Binding Protein G
  • [Other-IDs] NLM/ NIHMS285571; NLM/ PMC3166382
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4. |......... 1%  Bandyopadhyay D, Sen S: Disseminated cysticercosis with huge muscle hypertrophy. Indian J Dermatol; 2009;54(1):49-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disseminated cysticercosis with huge muscle hypertrophy.
  • The larvae are carried in the blood stream after penetrating the walls of the alimentary tract and they lodge in different tissues like the skin, skeletal muscles, brain, fundus and heart, to cause disseminated cysticercosis.
  • They may inhabit the muscles and cause muscular hypertrophy, which, at times, may assume gross proportions.

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  • (PMID = 20049270.001).
  • [ISSN] 1998-3611
  • [Journal-full-title] Indian journal of dermatology
  • [ISO-abbreviation] Indian J Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2800871
  • [Keywords] NOTNLM ; Cysticercosis / muscle hypertrophy / subcutaneous nodules
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5. |......... 1%  Saliba Y, Chouery E, Mégarbané A, Jabbour H, Farès N: Microalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats. Physiol Res; 2010;59(6):871-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats.
  • The objective of this study was to assess a possible link between microalbuminuria (MA), a major risk factor of the cardiorenal syndrome and the brain natriuretic peptide (BNP), a marker of cardiac hypertrophy.
  • Under drug treatment, decreases in blood pressure (p < 0.001), creatinine levels (p < 0.05), plasma TGF-β1 (p < 0.005) and BNP (p < 0.05) concentrations, were concomitant with the absence of MA which was significantly correlated with reductions in cardiac mass (p < 0.05) and hypertrophy markers (BNP and β-MHC gene expression) (p < 0.005) as well as in renal fibrosis.
  • These findings suggest a potential link between microalbuminuria evolution and BNP as well as a possible effect of microalbuminuria-lowering therapy on halting the progression, or even inducing the regression of cardiac hypertrophy.
  • [MeSH-major] Albuminuria / complications. Cardiomegaly / etiology. Hypertension / complications. Natriuretic Peptide, Brain / metabolism

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  • (PMID = 20533867.001).
  • [ISSN] 1802-9973
  • [Journal-full-title] Physiological research / Academia Scientiarum Bohemoslovaca
  • [ISO-abbreviation] Physiol Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1; 114471-18-0 / Natriuretic Peptide, Brain; AYI8EX34EU / Creatinine
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6. |......... 1%  Campos LA, Bader M, Baltatu OC: Brain Renin-Angiotensin system in hypertension, cardiac hypertrophy, and heart failure. Front Physiol; 2011;2:115
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain Renin-Angiotensin system in hypertension, cardiac hypertrophy, and heart failure.
  • Brain renin-angiotensin system (RAS) is significantly involved in the roles of the endocrine RAS in cardiovascular regulation.
  • Our studies indicate that the brain RAS participates in the development of cardiac hypertrophy and fibrosis through sympathetic activation.
  • Inhibition of sympathetic hyperactivity after myocardial infarction through suppression of the brain RAS appears beneficial.
  • Furthermore, the brain RAS modulates the cardiovascular and fluid-electrolyte homeostasis not only by interacting with the autonomic nervous system but also by modulating hypothalamic-pituitary axis and vasopressin release.
  • The brain RAS is also involved in the modulation of circadian rhythms of arterial pressure, contributing to non-dipping hypertension.
  • We conclude that the brain RAS in pathophysiological states interacts synergistically with the chronically overactive RAS through a positive biofeedback in order to maintain a state of alert in diseased conditions, such as cardiac hypertrophy and failure.
  • Therefore, targeting brain RAS with drugs such as renin or angiotensin converting enzyme inhibitors or receptor blockers having increased brain penetrability could be of advantage.

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  • (PMID = 22291657.001).
  • [ISSN] 1664-042X
  • [Journal-full-title] Frontiers in physiology
  • [ISO-abbreviation] Front Physiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3250059
  • [Keywords] NOTNLM ; angiotensin / brain / fibrosis / heart failure / hypertrophy / sympathetic nervous system
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7. |......... 1%  Feng B, Chen S, George B, Feng Q, Chakrabarti S: miR133a regulates cardiomyocyte hypertrophy in diabetes. Diabetes Metab Res Rev; 2010 Jan;26(1):40-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] miR133a regulates cardiomyocyte hypertrophy in diabetes.
  • BACKGROUND: Diabetic cardiomyopathy, characterized by cardiac hypertrophy and contractile dysfunction, eventually leads to heart failure.
  • We have previously shown that alterations of a number of key molecules are involved in producing cardiomyocyte hypertrophy in diabetes.
  • We further investigated neonatal rat cardiomyocytes to identify the mechanisms of glucose-induced hypertrophy and the potential role of miR133a.
  • RESULTS: Diabetic mice showed myocardial contractile dysfunction and augmented mRNA expression of atrial and brain natriuretic peptides (ANP, BNP), MEF2A and MEF2C, SGK1 and IGF1R compared to age- and sex-matched controls.
  • CONCLUSION: Data from these studies demonstrate a novel glucose-induced mechanism regulating gene expression and cardiomyocyte hypertrophy in diabetes which is mediated through miR133a.

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 20013939.001).
  • [ISSN] 1520-7560
  • [Journal-full-title] Diabetes/metabolism research and reviews
  • [ISO-abbreviation] Diabetes Metab. Res. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MADS Domain Proteins; 0 / MEF2 Transcription Factors; 0 / MEF2A protein, rat; 0 / MEF2C protein, rat; 0 / MicroRNAs; 0 / Myogenic Regulatory Factors
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8. |......... 1%  Cho HJ, Roh HG, Chun YI, Moon CT, Chung HW, Kim HY: Hypertrophy of the vasa vasorum: vascular response to the hungry brain. Neurologist; 2012 May;18(3):133-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypertrophy of the vasa vasorum: vascular response to the hungry brain.
  • Previous research documents revascularization through hypertrophy of the vasa vasorum after occlusion of the carotid artery.
  • However, the relationship between the cerebral vascular demands and the hypertrophy of the vasa vasorum has not been well delineated by functional studies.
  • In addition to the metabolic demand of the occluded vessel wall itself, the vascular demands of the hypoperfused brain may be a trigger factor that leads to hypertrophy of the vasa vasorum as collateral channels.
  • [MeSH-major] Brain / pathology. Infarction, Middle Cerebral Artery / pathology. Infarction, Middle Cerebral Artery / surgery. Vasa Vasorum / pathology. Vascular Surgical Procedures / methods
  • [MeSH-minor] Aged. Cerebral Angiography. Humans. Hypertrophy. Longitudinal Studies. Magnetic Resonance Imaging. Male. Tomography, Emission-Computed, Single-Photon

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  • (PMID = 22549353.001).
  • [ISSN] 1074-7931
  • [Journal-full-title] The neurologist
  • [ISO-abbreviation] Neurologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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9. |......... 1%  Xu H, Zhang Y, Sun J, Wei J, Sun L, Zhang J: Effect of distinct sources of Ca(2+) on cardiac hypertrophy in cardiomyocytes. Exp Biol Med (Maywood); 2012 Mar;237(3):271-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of distinct sources of Ca(2+) on cardiac hypertrophy in cardiomyocytes.
  • It is believed that intracellular calcium (Ca(2+)) overload can cause the cardiac hypertrophy, but it is possible that the Ca(2+) entering the cytoplasm through distinct pathways will induce various effects on cardiomyocytes.
  • The aim of the present study is to explore the effect of different sources of Ca(2+) on cardiomyocyte hypertrophy.
  • Caffeine and Ang II increased the cell surface area of cardiomyocytes and the mRNA level of atrial natriuretic peptide, brain natriuretic peptide and β-myosin heavy chain, but ionomycin did not.
  • Furthermore, cardiomyocyte hypertrophy induced by caffeine was inhibited by cyclosporin A (CsA) and KN93, whereas cardiomyocyte hypertrophy induced by Ang II was inhibited by KN93, but not CsA.
  • Our results show that cardiomyocyte hypertrophy is associated with SERCA2a activity, contractile performance and signaling pathways of CaMKII and/or calcineurin, whereas the Ca(2+) overload is not sufficient to cause the cardiomyocyte hypertrophy.

  • HSDB. structure - CALCIUM, ELEMENTAL.
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  • (PMID = 22345300.001).
  • [ISSN] 1535-3699
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 3.1.3.16 / Calcineurin; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium
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10. |......... 1%  Liu J, Hao DD, Zhang JS, Zhu YC: Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a. Biochem Biophys Res Commun; 2011 Sep 23;413(2):342-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a.
  • However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH).
  • Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes.
  • [MeSH-minor] Animals. Cell Line. Hypertrophy / metabolism. Hypertrophy / pathology. Natriuretic Peptide, Brain / biosynthesis. Natriuretic Peptide, Brain / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Reactive Oxygen Species / metabolism. Sulfides / pharmacology. Up-Regulation

  • HSDB. structure - SODIUM HYDROSULFIDE.
  • HSDB. structure - HYDROGEN SULFIDE.
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  • [Copyright] Copyright © 2011 Elsevier Inc. All rights reserved.
  • (PMID = 21893044.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN133 microRNA, rat; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Sulfides; 114471-18-0 / Natriuretic Peptide, Brain; FWU2KQ177W / sodium bisulfide; YY9FVM7NSN / Hydrogen Sulfide
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11. |......... 1%  Kang BY, Wang W, Palade P, Sharma SG, Mehta JL: Cardiac hypertrophy during hypercholesterolemia and its amelioration with rosuvastatin and amlodipine. J Cardiovasc Pharmacol; 2009 Oct;54(4):327-34
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  • [Title] Cardiac hypertrophy during hypercholesterolemia and its amelioration with rosuvastatin and amlodipine.
  • Hypercholesterolemia is a common accompaniment of atherosclerosis and may be associated with cardiac hypertrophy.
  • To define the mechanistic basis of cardiac hypertrophy in hypercholesterolemia, we fed low-density lipoprotein receptor knockout (LDLR KO) mice regular diet or high cholesterol (HC) diet for 26 weeks.
  • There was clear evidence of cardiomyocyte hypertrophy and collagen deposition in the hearts of LDLR KO mice fed with HC diet, confirmed by histopathology (hematoxylin and eosin and Picrosirius staining) and upregulation of genes for brain natriuretic peptide, alpha-tubulin, transforming growth factor beta1, and connective tissue growth factor (CTGF).
  • These phenomena were associated with a marked decrease in cardiomyocyte hypertrophy and collagen deposits in and around the cardiomyocytes.
  • In conclusion, this study provides evidence of cardiac hypertrophy and fibrosis in hypercholesterolemia independent of blood pressure change LOX-1 and AT1R act as possible signals for oxidant stress leading to alterations in cardiac structure during hypercholesterolemia.
  • Most importantly, rosuvastatin and amlodipine ameliorate cardiomyocyte hypertrophy and fibrosis.

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  • (PMID = 19687748.001).
  • [ISSN] 1533-4023
  • [Journal-full-title] Journal of cardiovascular pharmacology
  • [ISO-abbreviation] J. Cardiovasc. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Cholesterol, Dietary; 0 / Fluorobenzenes; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Lipids; 0 / Pyrimidines; 0 / Receptors, LDL; 0 / Sulfonamides; 1J444QC288 / Amlodipine; 287714-41-4 / rosuvastatin
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12. |......... 1%  Sonmez G, Uzun G, Mutluoglu M, Toklu AS, Mutlu H, Ay H, Yildiz S: Paranasal sinus mucosal hypertrophy in experienced divers. Aviat Space Environ Med; 2011 Oct;82(10):992-4
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  • [Title] Paranasal sinus mucosal hypertrophy in experienced divers.
  • Although not as important as dysbaric osteonecrosis, ischemic brain lesions, or neurophysiological symptoms, paranasal sinus mucosal hypertrophy (PSMH) has also been discussed as being more prevalent among divers.
  • [MeSH-minor] Adult. Case-Control Studies. Humans. Hypertrophy. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 21961405.001).
  • [ISSN] 0095-6562
  • [Journal-full-title] Aviation, space, and environmental medicine
  • [ISO-abbreviation] Aviat Space Environ Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. |......... 1%  Elliott MB, Jallo JJ, Barbe MF, Tuma RF: Hypertonic saline attenuates tissue loss and astrocyte hypertrophy in a model of traumatic brain injury. Brain Res; 2009 Dec 11;1305:183-91
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  • [Title] Hypertonic saline attenuates tissue loss and astrocyte hypertrophy in a model of traumatic brain injury.
  • The role of astrocyte responses after traumatic brain injury remains unclear.
  • There is evidence that reduced astrocyte proliferation is detrimental while increased hypertrophy and proliferation are signs of increased injury severity.
  • Therefore, this study focused on the hypothesis that hypertonic saline-induced improvements in histological outcome are time dependent and may be associated with alterations in astrocyte hypertrophy after cortical contusion injury.
  • Brain tissue loss determined using cresyl violet staining and astrocyte hypertrophy and proliferation were assessed using glial fibrillary acidic protein immunostaining in hypertonic saline and normal saline treated rats, and untreated, injured controls.
  • Results show that hypertonic saline treatment reduced tissue loss that correlated with attenuated astrocyte hypertrophy characterized by reductions in astrocyte immunoreactivity without changes in the number of astrocytes after CCI injury.
  • Delayed treatment of hypertonic saline resulted in the greatest reduction in tissue loss compared to all other treatments indicating that there is a therapeutic window for hypertonic saline use after traumatic brain injury.
  • [MeSH-major] Astrocytes / drug effects. Brain Injuries / drug therapy. Cell Enlargement / drug effects. Cerebral Cortex / drug effects. Saline Solution, Hypertonic / therapeutic use

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  • (PMID = 19804766.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / U01 HD042738
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Saline Solution, Hypertonic
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14. |......... 1%  Sumbalová Z, Kucharská J, Kristek F: Losartan improved respiratory function and coenzyme Q content in brain mitochondria of young spontaneously hypertensive rats. Cell Mol Neurobiol; 2010 Jul;30(5):751-8
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  • [Title] Losartan improved respiratory function and coenzyme Q content in brain mitochondria of young spontaneously hypertensive rats.
  • This study examined the impact of hypertension on mitochondrial respiratory chain function, coenzyme Q(9) (CoQ(9)), coenzyme Q(10) (CoQ(10)), and alpha-tocopherol content in brain mitochondria, and the effect of blockade of angiotensin II type 1 receptors (AT1R) in the prehypertensive period on these parameters.
  • In addition, blood pressure, heart and brain weight to body weight ratios, and the geometry of the basilar artery supplying the brain were evaluated.
  • In the 9th week blood pressure and heart weight/body weight ratio were significantly increased and brain weight/body weight ratio was significantly decreased in spontaneously hypertensive rats (SHR) when compared to Wistar rats (WR).
  • The treatment of SHR with losartan (20 mg/kg/day) from 4th to 9th week of age exerted preventive effect against hypertension, heart and arterial wall hypertrophy, and brain weight/body weight decline.
  • The impairment of energy production and decreased level of lipid-soluble antioxidants in brain mitochondria as well as structural alterations in the basilar artery may contribute to increased vulnerability of brain tissue in hypertension.
  • Long-term treatment with AT1R blockers may prevent brain dysfunction in hypertension.
  • [MeSH-major] Aging / drug effects. Angiotensin II Type 1 Receptor Blockers / pharmacology. Brain / metabolism. Losartan / pharmacology. Mitochondria / drug effects. Mitochondria / metabolism. Ubiquinone / metabolism

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  • (PMID = 20145991.001).
  • [ISSN] 1573-6830
  • [Journal-full-title] Cellular and molecular neurobiology
  • [ISO-abbreviation] Cell. Mol. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Antioxidants; 0 / Glutamates; 03L9OT429T / Rotenone; 1339-63-5 / Ubiquinone; 303-98-0 / coenzyme Q10; AB6MNQ6J6L / Succinic Acid; EC 1.9.3.1 / Electron Transport Complex IV; H4N855PNZ1 / alpha-Tocopherol; JMS50MPO89 / Losartan
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15. |......... 1%  Ramakrishna R, Mai JC, Filardi T, Browd SR, Ellenbogen RG: Brainstem hypertrophy, acquired Chiari malformation, syringomyelia, and hydrocephalus: diagnostic dilemma. J Neurosurg Pediatr; 2011 Aug;8(2):184-8
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  • [Title] Brainstem hypertrophy, acquired Chiari malformation, syringomyelia, and hydrocephalus: diagnostic dilemma.
  • Repeat neural axis imaging revealed resolution of the syrinx but prominent brainstem hypertrophy.
  • Eventually, the placement of a ventriculoperitoneal shunt resulted in the resolution of both symptoms and brainstem hypertrophy.
  • In the present article, the authors elaborate on this first reported case of a reversible brainstem hypertrophy responsive to CSF shunting.
  • [MeSH-major] Arnold-Chiari Malformation / pathology. Brain Stem / pathology. Hydrocephalus / pathology. Postoperative Complications / pathology. Syringomyelia / pathology
  • [MeSH-minor] Adolescent. Cerebral Hemorrhage / surgery. Cerebrospinal Fluid Shunts. Decompression, Surgical / adverse effects. Encephalomalacia / pathology. Encephalomalacia / surgery. Female. Humans. Hypertrophy. Magnetic Resonance Imaging. Reoperation


16. |......... 1%  Bhavsar PK, Brand NJ, Felkin LE, Luther PK, Cullen ME, Yacoub MH, Barton PJ: Clenbuterol induces cardiac myocyte hypertrophy via paracrine signalling and fibroblast-derived IGF-1. J Cardiovasc Transl Res; 2010 Dec;3(6):688-95
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  • [Title] Clenbuterol induces cardiac myocyte hypertrophy via paracrine signalling and fibroblast-derived IGF-1.
  • The β(2)-selective adrenoreceptor agonist clenbuterol promotes both skeletal and cardiac muscle hypertrophy and is undergoing clinical trials in the treatment of muscle wasting and heart failure.
  • We have previously demonstrated that clenbuterol induces a mild physiological ventricular hypertrophy in vivo with normal contractile function and without induction of α-skeletal muscle actin (αSkA), a marker of pathological hypertrophy.
  • Real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) revealed elevated mRNA expression of ANP and brain natriuretic peptide (BNP) but without change in αSkA, consistent with physiological hypertrophic growth.
  • Together these data show that clenbuterol acts to induce mild cardiac hypertrophy in cardiac myocytes via paracrine signalling involving fibroblast-derived IGF-1.
  • [MeSH-minor] Actins / genetics. Animals. Animals, Newborn. Atrial Natriuretic Factor / genetics. Blotting, Western. Cell Size / drug effects. Cells, Cultured. Gene Expression Regulation. Natriuretic Peptide, Brain / genetics. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Protein Kinase Inhibitors. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transfection

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  • (PMID = 20577844.001).
  • [ISSN] 1937-5395
  • [Journal-full-title] Journal of cardiovascular translational research
  • [ISO-abbreviation] J Cardiovasc Transl Res
  • [Language] eng
  • [Grant] United Kingdom / British Heart Foundation / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Adrenergic beta-2 Receptor Agonists; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 0 / insulin-like growth factor-1, rat; 114471-18-0 / Natriuretic Peptide, Brain; 67763-96-6 / Insulin-Like Growth Factor I; 85637-73-6 / Atrial Natriuretic Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; XTZ6AXU7KN / Clenbuterol
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17. |......... 1%  Chan SL, Baumbach GL: Nox2 deficiency prevents hypertension-induced vascular dysfunction and hypertrophy in cerebral arterioles. Int J Hypertens; 2013;2013:793630
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  • [Title] Nox2 deficiency prevents hypertension-induced vascular dysfunction and hypertrophy in cerebral arterioles.
  • Oxidative stress is involved in many hypertension-related vascular diseases in the brain, including stroke and dementia.
  • L-NAME reduced dilation to acetylcholine but did not result in hypertrophy in right-sided arterioles of Nox2-/y  mice.
  • In conclusion, hypertension-induced superoxide production derived from Nox2-containing NADPH oxidase promotes hypertrophy and causes endothelial dysfunction in cerebral arterioles, possibly involving interaction with nitric oxide.

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  • (PMID = 23573415.001).
  • [ISSN] 2090-0384
  • [Journal-full-title] International journal of hypertension
  • [ISO-abbreviation] Int J Hypertens
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS072628
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3612447
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18. |......... 1%  Zhang L, Corona-Morales AA, Vega-González A, García-Estrada J, Escobar A: Dietary tryptophan restriction in rats triggers astrocyte cytoskeletal hypertrophy in hippocampus and amygdala. Neurosci Lett; 2009 Feb 6;450(3):242-5
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  • [Title] Dietary tryptophan restriction in rats triggers astrocyte cytoskeletal hypertrophy in hippocampus and amygdala.
  • Due to astrocyte involvement in critical brain mechanisms, it seems worth to investigate possible adaptive changes in the glial population with TRP restriction.
  • Antibody against glial fibrillary acidic protein (GFAP), a principal intermediate filament in astrocytes, was used to evaluate cytoskeletal hypertrophy and glial proliferation.
  • [MeSH-major] Astrocytes / pathology. Brain / pathology. Cytoskeleton / pathology. Food, Formulated / adverse effects. Malnutrition / pathology. Tryptophan / deficiency
  • [MeSH-minor] Amygdala / metabolism. Amygdala / pathology. Amygdala / physiopathology. Animals. Biological Markers / metabolism. Cell Shape / physiology. Glial Fibrillary Acidic Protein / metabolism. Gliosis / metabolism. Gliosis / pathology. Gliosis / physiopathology. Hippocampus / metabolism. Hippocampus / pathology. Hippocampus / physiopathology. Hypertrophy / metabolism. Hypertrophy / pathology. Hypertrophy / physiopathology. Male. Rats. Rats, Wistar. Serotonin / biosynthesis. Serotonin / deficiency

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  • (PMID = 19095041.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biological Markers; 0 / Glial Fibrillary Acidic Protein; 333DO1RDJY / Serotonin; 8DUH1N11BX / Tryptophan
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19. |......... 1%  Barbosa AF, Raggi GC, Sá Cdos S, Costa MP, Lima Jr JE, Tanaka C: Postural control in women with breast hypertrophy. Clinics (Sao Paulo); 2012 Jul;67(7):757-60
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  • [Title] Postural control in women with breast hypertrophy.
  • OBJECTIVES: The consequences of breast hypertrophy have been described based on the alteration of body mass distribution, leading to an impact on psychological and physical aspects.
  • The principles of motor control suggest that breast hypertrophy can lead to sensorimotor alterations and the impairment of body balance due to postural misalignment.
  • The aim of this study is to evaluate the postural control of women with breast hypertrophy under different sensory information conditions.
  • METHOD: This cross-sectional study included 14 women with breast hypertrophy and 14 without breast hypertrophy, and the mean ages of the groups were 39 ± 15 years and 39 ± 16 years, respectively.
  • RESULTS: Women with breast hypertrophy presented an area that was significantly higher for three out of four conditions and a higher velocity of center of pressure displacement in the anterior-posterior direction under two conditions: eyes open and mobile platform and eyes closed and mobile platform.
  • CONCLUSIONS: Women with breast hypertrophy have altered postural control, which was demonstrated by the higher area and velocity of center of pressure displacement.
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Cross-Sectional Studies. Female. Humans. Hypertrophy / physiopathology. Middle Aged. Young Adult

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  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
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  • [Other-IDs] NLM/ PMC3400165
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20. |......... 1%  Zhao Y, Wang C, Wu J, Wang Y, Zhu W, Zhang Y, Du Z: Choline protects against cardiac hypertrophy induced by increased after-load. Int J Biol Sci; 2013;9(3):295-302
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  • [Title] Choline protects against cardiac hypertrophy induced by increased after-load.
  • BACKGROUND: Although inadequate intake of essential nutrient choline has been known to significantly increase cardiovascular risk, whether additional supplement of choline offering a protection against cardiac hypertrophy remain unstudied.
  • METHODS: The effects of choline supplements on pathological cardiac hypertrophic growth induced by transverse aorta constriction (TAC) for three weeks and cardiomyocyte hypertrophy in cultured cells induced by isoproterenol (ISO) 10 μM for 48 h stimulation were investigated.
  • RESULTS: Administration of 14 mg/kg choline to mice undergone TAC effectively attenuated the cardiac hypertrophic responses, as indicated by the reduced heart weight, left ventricular weight, ventricular thickness, and reduced expression of biomarker genes of cardiac hypertrophy.
  • This anti-hypertrophic efficacy was reproduced in a cellular model of cardiomyocyte hypertrophy induced by isoproterenol in cultured neonatal cardiomyocytes.
  • Our results further showed that choline rescued the aberrant downregulation of the muscle-specific microRNA miR-133a expression, a recently identified anti-hypertrophic factor, and restored the elevated calcineurin protein level, the key signaling molecule for the development of cardiac hypertrophy.
  • CONCLUSION: Our study unraveled for the first time the cardioprotection of choline against cardiac hypertrophy, with correction of expression of miR-133a and calcineurin as a possible mechanism.
  • Our findings suggest that choline supplement may be considered for adjunct anti-hypertrophy therapy.

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  • (PMID = 23493786.001).
  • [ISSN] 1449-2288
  • [Journal-full-title] International journal of biological sciences
  • [ISO-abbreviation] Int. J. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 0 / Genetic Markers; 0 / MicroRNAs; 0 / Mirn133 microRNA, mouse; EC 3.1.3.16 / Calcineurin; L628TT009W / Isoproterenol; N91BDP6H0X / Choline
  • [Other-IDs] NLM/ PMC3596715
  • [Keywords] NOTNLM ; Calcineurin. / cardiac hypertrophy / cardiomyocyte / choline / miR-133a
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21. |......... 1%  Lu JC, Cui W, Zhang HL, Liu F, Han M, Liu DM, Yin HN, Zhang K, Du J: Additive beneficial effects of amlodipine and atorvastatin in reversing advanced cardiac hypertrophy in elderly spontaneously hypertensive rats. Clin Exp Pharmacol Physiol; 2009 Nov;36(11):1110-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Additive beneficial effects of amlodipine and atorvastatin in reversing advanced cardiac hypertrophy in elderly spontaneously hypertensive rats.
  • However, it is still unclear whether the combination of amlodipine and atorvastatin has additive beneficial effects on the regression of advanced cardiac hypertrophy in hypertension.
  • In the present study, the effects of the drug combination on advanced cardiac hypertrophy were investigated in elderly spontaneously hypertensive rats (SHR).
  • 3. Combined administration of amlodipine and atorvastatin significantly suppressed cardiomyocyte hypertrophy, interstitial fibrosis and upregulation of hypertrophic and profibrotic genes, and also improved left ventricular diastolic dysfunction to a greater extent than did amlodipine monotherapy.
  • Further beneficial effects of combination therapy on advanced cardiac hypertrophy were associated with a greater reduction of NADPH oxidase-mediated increases in cardiac reactive oxygen species (ROS), rather than decreased blood pressure and serum cholesterol levels.
  • 5. In conclusion, combined amlodipine and atorvastatin treatment has a greater beneficial effect on advanced cardiac hypertrophy compared with amlodipine monotherapy.
  • [MeSH-minor] Animals. Drug Synergism. Drug Therapy, Combination. Fibrosis / metabolism. Hemodynamics / drug effects. Myocytes, Cardiac / pathology. NADPH Oxidase / metabolism. Natriuretic Peptide, Brain / metabolism. Oxidative Stress / drug effects. Random Allocation. Rats. Rats, Inbred SHR. Reactive Oxygen Species / metabolism. Superoxide Dismutase / metabolism. Ventricular Dysfunction, Left / metabolism. Ventricular Dysfunction, Left / physiopathology


22. |......... 1%  Moubarak M, Jabbour H, Smayra V, Chouery E, Saliba Y, Jebara V, Fares N: Cardiorenal syndrome in hypertensive rats: microalbuminuria, inflammation and ventricular hypertrophy. Physiol Res; 2012;61(1):13-24
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  • [Title] Cardiorenal syndrome in hypertensive rats: microalbuminuria, inflammation and ventricular hypertrophy.
  • The aim of our study was to evaluate a possible association between microalbuminuria (MA), several low-grade inflammation factors and left ventricular hypertrophy (LVH) by using a pharmacological approach.
  • Rats in the 2K-1C group had all developed hypertension, a significant increase in plasma levels of tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), brain natriuretic peptide (BNP) and C-reactive protein (CRP).
  • These results were related to the absence of MA which was significantly associated with reductions in cardiac mass and hypertrophy markers (BNP and beta-MHC gene expression) as well as renal interstitial inflammation.
  • In conclusion, our results suggest that the reduction of MA is correlated with the decrease of the inflammatory components and seems to play an important role in protecting against cardiac hypertrophy and renal injury.
  • [MeSH-major] Albuminuria / metabolism. Cardio-Renal Syndrome / metabolism. Hypertrophy, Left Ventricular / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 22188107.001).
  • [ISSN] 1802-9973
  • [Journal-full-title] Physiological research / Academia Scientiarum Bohemoslovaca
  • [ISO-abbreviation] Physiol Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 9007-41-4 / C-Reactive Protein
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23. |......... 1%  Ye Y, Mou Y, Bai B, Li L, Chen GP, Hu SJ: Knockdown of farnesylpyrophosphate synthase prevents angiotensin II-mediated cardiac hypertrophy. Int J Biochem Cell Biol; 2010 Dec;42(12):2056-64
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  • [Title] Knockdown of farnesylpyrophosphate synthase prevents angiotensin II-mediated cardiac hypertrophy.
  • The Rho guanosine triphosphatases (Rho GTPases) family, including RhoA, plays an important role in angiotensin II (Ang II)-mediated cardiac hypertrophy.
  • The present study was designed to investigate the role of FPPS in myocardial hypertrophy mediated with Ang II.
  • Successful FPPS silencing in NCMs completely inhibited the hypertrophy marker genes of β-myosin heavy chain (β-MHC) and brain natriuretic peptide (BNP), as well as cell surface area.
  • In conclusion, FPPS with RhoA associated p-38 and JNK MAPK signaling might play an important role in Ang II-induced cardiac hypertrophy.

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20884373.001).
  • [ISSN] 1878-5875
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 11128-99-7 / Angiotensin II; EC 2.5.1.1 / Dimethylallyltranstransferase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 3.6.5.2 / rhoA GTP-Binding Protein
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24. |......... 1%  Woo JS, Cho CH, Lee KJ, Kim do H, Ma J, Lee EH: Hypertrophy in skeletal myotubes induced by junctophilin-2 mutant, Y141H, involves an increase in store-operated Ca2+ entry via Orai1. J Biol Chem; 2012 Apr 27;287(18):14336-48
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  • [Title] Hypertrophy in skeletal myotubes induced by junctophilin-2 mutant, Y141H, involves an increase in store-operated Ca2+ entry via Orai1.
  • We previously reported that S165F also induced both hypertrophy and altered intracellular Ca(2+) signaling in mouse skeletal myotubes.
  • Consistent with S165F, Y141H led to hypertrophy and altered Ca(2+) signaling (a decrease in the gain of excitation-contraction coupling and an increase in the resting level of myoplasmic Ca(2+)).
  • Instead, abnormal JMC and increased SOCE via Orai1 were found, suggesting that the hypertrophy caused by Y141H progressed differently from S165F.
  • Therefore JP2 can be linked to skeletal muscle hypertrophy via various Ca(2+) signaling pathways, and SOCE could be one of the causes of altered Ca(2+) signaling observed in muscle hypertrophy.

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  • (PMID = 22389502.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Membrane Proteins; 0 / Muscle Proteins; 0 / ORAI1 protein, human; 0 / Orai1 protein, mouse; 0 / Ryanodine Receptor Calcium Release Channel; 0 / junctophilin; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC3340289
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25. |......... 1%  Horikawa YT, Panneerselvam M, Kawaraguchi Y, Tsutsumi YM, Ali SS, Balijepalli RC, Murray F, Head BP, Niesman IR, Rieg T, Vallon V, Insel PA, Patel HH, Roth DM: Cardiac-specific overexpression of caveolin-3 attenuates cardiac hypertrophy and increases natriuretic peptide expression and signaling. J Am Coll Cardiol; 2011 May 31;57(22):2273-83
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  • [Title] Cardiac-specific overexpression of caveolin-3 attenuates cardiac hypertrophy and increases natriuretic peptide expression and signaling.
  • OBJECTIVES: We hypothesized that cardiac myocyte-specific overexpression of caveolin-3 (Cav-3), a muscle-specific caveolin, would alter natriuretic peptide signaling and attenuate cardiac hypertrophy.
  • BACKGROUND: Natriuretic peptides modulate cardiac hypertrophy and are potential therapeutic options for patients with heart failure.
  • Caveolae, microdomains in the plasma membrane that contain caveolin proteins and natriuretic peptide receptors, have been implicated in cardiac hypertrophy and natriuretic peptide localization.
  • RESULTS: The Cav-3 OE mice subjected to transverse aortic constriction had increased survival, reduced cardiac hypertrophy, and maintenance of cardiac function compared with control mice.
  • In left ventricle at baseline, messenger ribonucleic acid for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were increased 7- and 3-fold, respectively, in Cav-3 OE mice compared with control subjects and were accompanied by increased protein expression for ANP and BNP.
  • CONCLUSIONS: These results imply that cardiac myocyte-specific Cav-3 OE is a novel strategy to enhance natriuretic peptide expression, attenuate hypertrophy, and possibly exploit the therapeutic benefits of natriuretic peptides in cardiac hypertrophy and heart failure.
  • [MeSH-major] Atrial Natriuretic Factor / metabolism. Cardiomegaly / metabolism. Caveolae / metabolism. Caveolin 3 / metabolism. Myocytes, Cardiac / metabolism. Natriuretic Peptide, Brain / metabolism

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  • [Copyright] Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 21616289.001).
  • [ISSN] 1558-3597
  • [Journal-full-title] Journal of the American College of Cardiology
  • [ISO-abbreviation] J. Am. Coll. Cardiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK079337; United States / NIGMS NIH HHS / GM / GM007198; United States / NIGMS NIH HHS / GM / GM66232; United States / NHLBI NIH HHS / HL / HL007261; United States / NHLBI NIH HHS / HL / HL081400; United States / NHLBI NIH HHS / HL / HL091071; United States / NHLBI NIH HHS / HL / HL094728; United States / NHLBI NIH HHS / HL / HL66941; United States / NHLBI NIH HHS / HL / R00 HL091061-04; United States / NHLBI NIH HHS / HL / R01 HL081400-04
  • [Publication-type] In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caveolin 3; 0 / NFATC Transcription Factors; 0 / RNA, Messenger; 0 / transcription factor NF-AT c3; 114471-18-0 / Natriuretic Peptide, Brain; 85637-73-6 / Atrial Natriuretic Factor; H2D2X058MU / Cyclic GMP
  • [Other-IDs] NLM/ NIHMS341681; NLM/ PMC3236642
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26. |......... 1%  Coutinho T, Al-Omari M, Mosley TH Jr, Kullo IJ: Biomarkers of left ventricular hypertrophy and remodeling in blacks. Hypertension; 2011 Nov;58(5):920-5
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  • [Title] Biomarkers of left ventricular hypertrophy and remodeling in blacks.
  • Left ventricular (LV) hypertrophy, a marker for adverse cardiovascular events, is more common in blacks than in non-Hispanic whites.
  • Mechanisms leading to LV hypertrophy and mediating its clinical sequelae in blacks are not fully understood.
  • LV mass was measured by transthoracic echocardiography and indexed to height.(2.7) LV geometry was categorized as normal, concentric remodeling, concentric hypertrophy, and eccentric hypertrophy.
  • After adjustment for potential confounders, log-transformed levels of the following biomarkers were independently associated with LV mass index: N-terminal pro-brain natriuretic peptide (β±SE=0.07±0.01 pg/mL; P<0.0001), mid-regional pro-atrial natriuretic peptide (β±SE=0.08±0.02 pmol/L; P<0.0001), mid-regional pro-adrenomedullin (β±SE=0.09±0.03 nmol/L; P=0.0006), C-terminal pro-endothelin (β± SE=0.05±0.02 pmol/L; P=0.0009), and osteoprotegerin (β±SE=0.07±0.02 pg/mL; P=0.0005) (β is for 1 log increase in biomarker level).
  • The associations of these biomarkers with LV mass index were mainly due to their association with eccentric hypertrophy.
  • Higher circulating levels of natriuretic peptides, adrenomedullin, endothelin, and osteoprotegerin were associated with increased LV mass index, providing insights into the pathophysiology of LV hypertrophy in blacks.
  • [MeSH-major] African Americans / statistics & numerical data. Biological Markers / blood. Hypertrophy, Left Ventricular / blood. Hypertrophy, Left Ventricular / ethnology. Ventricular Remodeling / physiology

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  • (PMID = 21986506.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL81331; United States / NHLBI NIH HHS / HL / R01 HL089354; United States / NHLBI NIH HHS / HL / R01 HL089354-02; United States / NHLBI NIH HHS / HL / U01 HL081331; United States / NHLBI NIH HHS / HL / U01 HL081331-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biological Markers; 0 / Natriuretic Peptides
  • [Other-IDs] NLM/ NIHMS331849; NLM/ PMC3249445
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27. |......... 1%  Purushothaman S, Renuka Nair R, Harikrishnan VS, Fernandez AC: Temporal relation of cardiac hypertrophy, oxidative stress, and fatty acid metabolism in spontaneously hypertensive rat. Mol Cell Biochem; 2011 May;351(1-2):59-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temporal relation of cardiac hypertrophy, oxidative stress, and fatty acid metabolism in spontaneously hypertensive rat.
  • Left ventricular hypertrophy is an adaptive response to hypertension, and an independent clinical risk factor for cardiac failure, sudden death, and myocardial infarction.
  • As regression of cardiac hypertrophy is associated with a lower likelihood of cardiovascular events, it is recognized as a target of antihypertensive therapy.
  • This necessitates identification of factors associated with the initiation and progression of hypertrophy.
  • Oxidative stress and metabolic shift are intimately linked with myocardial hypertrophy, but their interrelationship is not clearly understood.
  • This study proposes to identify the temporal sequence of events so as to distinguish whether oxidative stress and metabolic shift are a cause or consequence of hypertrophy.
  • Cardiac hypertrophy was apparent at 2 months of age, as assessed by hypertrophy index and brain natriuretic peptide gene expression.
  • Enhanced myocardial lipid peroxidation accompanied by nuclear factor-kappa B gene expression in one-month-old SHR suggests that oxidative stress precedes the development of hypertrophy.
  • Metabolic shift identified by reduction in the expression of peroxisome proliferator-activated receptor-alpha, medium chain acyl CoA dehydrogenase, and carnitine palmitoyltransferase 1β was seen at 4 months of age, implying that reduction of fatty acid oxidation is a consequence of hypertrophy.
  • Information on the temporal sequence of events associated with hypertrophy will help in the prevention and reversal of cardiac remodeling.
  • Investigations aimed at prevention of hypertrophy should address reduction of oxidative stress.
  • Both, oxidative stress and metabolic modulation have to be considered for studies that focus on the regression of hypertrophy.

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  • (PMID = 21264498.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Fatty Acids
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28. |......... 1%  Tan X, Li J, Wang X, Chen N, Cai B, Wang G, Shan H, Dong D, Liu Y, Li X, Yang F, Li X, Zhang P, Li X, Yang B, Lu Y: Tanshinone IIA protects against cardiac hypertrophy via inhibiting calcineurin/NFATc3 pathway. Int J Biol Sci; 2011;7(3):383-9
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  • [Title] Tanshinone IIA protects against cardiac hypertrophy via inhibiting calcineurin/NFATc3 pathway.
  • Pathological cardiac hypertrophy induced by adrenergic overactivation can subsequently develop to heart failure which remains as a leading cause of mortality worldwide.
  • However, little is know about the effect of Tanshinone IIA on cardiac hypertrophy.
  • The present study was aimed to investigate whether Tanshinone IIA prevents cardiac hypertrophy induced by isoproterenol (ISO) and to clarify its possible mechanisms.
  • Cardiomyocytes hypertrophy was induced by ISO 10 μM for 48 h with or without Tanshinone IIA 10, 30, 100 μM pretreatment, and evaluated by determining the cell size and the expression of ANP, BNP, β-MHC, Calcineurin, and NFATc3 by real-time PCR and western blot.
  • In summary, Tanshinone IIA attenuated cardiomyocyte hypertrophy induced by ISO through inhibiting Calcineurin/NFATc3 pathway, which provides new insights into the pharmacological role and therapeutic mechanism of Tanshinone IIA in heart diseases.
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / genetics. Atrial Natriuretic Factor / metabolism. Calcium Signaling / drug effects. Isoproterenol. Medicine, Chinese Traditional. Myocytes, Cardiac / drug effects. Myosin Heavy Chains / genetics. Myosin Heavy Chains / metabolism. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism. RNA, Messenger / metabolism. Rats. Up-Regulation / drug effects

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  • (PMID = 21494433.001).
  • [ISSN] 1449-2288
  • [Journal-full-title] International journal of biological sciences
  • [ISO-abbreviation] Int. J. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Bmyo protein, rat; 0 / Diterpenes, Abietane; 0 / Drugs, Chinese Herbal; 0 / NFATC Transcription Factors; 0 / RNA, Messenger; 114471-18-0 / Natriuretic Peptide, Brain; 568-73-0 / tanshinone; 85637-73-6 / Atrial Natriuretic Factor; EC 3.1.3.16 / Calcineurin; EC 3.6.4.1 / Myosin Heavy Chains; L628TT009W / Isoproterenol
  • [Other-IDs] NLM/ PMC3076506
  • [Keywords] NOTNLM ; Calcineurin / Cardiac hypertrophy / Isoproterenol / NFATc3 / Tanshinone IIA
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29. |......... 1%  Choi HJ, Nepal M, Park YR, Lee HK, Oh SR, Soh Y: Stimulation of chondrogenesis in ATDC5 chondroprogenitor cells and hypertrophy in mouse by Genkwadaphnin. Eur J Pharmacol; 2011 Mar 25;655(1-3):9-15
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  • [Title] Stimulation of chondrogenesis in ATDC5 chondroprogenitor cells and hypertrophy in mouse by Genkwadaphnin.
  • The control of chondrogenic differentiation and hypertrophy is critical for these processes.
  • [MeSH-minor] Alkaline Phosphatase / metabolism. Animals. Biological Markers / metabolism. Bone Diseases / drug therapy. Cartilage / drug effects. Cartilage / growth & development. Cell Differentiation / drug effects. Cell Line. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation / drug effects. Growth Plate / cytology. Growth Plate / drug effects. Hypertrophy / physiopathology. JNK Mitogen-Activated Protein Kinases / metabolism. Male. Mice. Proteoglycans / metabolism. Tibia / cytology. Tibia / drug effects. Tibia / growth & development

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  • [Copyright] Copyright © 2011 Elsevier B.V. All rights reserved.
  • (PMID = 21266170.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biological Markers; 0 / Diterpenes; 0 / Proteoglycans; 55073-32-0 / genkwadaphnin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.1.3.1 / Alkaline Phosphatase
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30. |......... 1%  Lin EQ, Irvine JC, Cao AH, Alexander AE, Love JE, Patel R, McMullen JR, Kaye DM, Kemp-Harper BK, Ritchie RH: Nitroxyl (HNO) stimulates soluble guanylyl cyclase to suppress cardiomyocyte hypertrophy and superoxide generation. PLoS One; 2012;7(4):e34892
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  • [Title] Nitroxyl (HNO) stimulates soluble guanylyl cyclase to suppress cardiomyocyte hypertrophy and superoxide generation.
  • BACKGROUND: New therapeutic targets for cardiac hypertrophy, an independent risk factor for heart failure and death, are essential.
  • The impact of HNO on cardiac hypertrophy (which is negatively regulated by cGMP) however has not been investigated.
  • CONCLUSIONS: Our results demonstrate that HNO prevents cardiomyocyte hypertrophy, and that cGMP-dependent NADPH oxidase suppression contributes to these antihypertrophic actions.
  • HNO donors may thus represent innovative pharmacotherapy for cardiac hypertrophy.
  • [MeSH-minor] Angiotensin II / adverse effects. Animals. Cell Adhesion Molecules / metabolism. Cyclic GMP / metabolism. Endothelin-1 / metabolism. Microfilament Proteins / metabolism. NADPH Oxidase / metabolism. Natriuretic Peptide, Brain / metabolism. Nitrites / pharmacology. Phosphoproteins / metabolism. Phosphorylation / drug effects. Rats. Reactive Oxygen Species / antagonists & inhibitors. Reactive Oxygen Species / metabolism. Signal Transduction / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 22506056.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Endothelin-1; 0 / Microfilament Proteins; 0 / Nitrites; 0 / Nitrogen Oxides; 0 / Phosphoproteins; 0 / Reactive Oxygen Species; 0 / Receptors, Cytoplasmic and Nuclear; 0 / vasodilator-stimulated phosphoprotein; 11062-77-4 / Superoxides; 11128-99-7 / Angiotensin II; 114471-18-0 / Natriuretic Peptide, Brain; 14332-28-6 / nitroxyl; 18550-55-5 / oxyhyponitrite; EC 1.6.3.1 / NADPH Oxidase; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 4.6.1.2 / Guanylate Cyclase; EC 4.6.1.2 / soluble guanylyl cyclase; H2D2X058MU / Cyclic GMP
  • [Other-IDs] NLM/ PMC3323591
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31. |......... 1%  Landstrom AP, Kellen CA, Dixit SS, van Oort RJ, Garbino A, Weisleder N, Ma J, Wehrens XH, Ackerman MJ: Junctophilin-2 expression silencing causes cardiocyte hypertrophy and abnormal intracellular calcium-handling. Circ Heart Fail; 2011 Mar;4(2):214-23
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  • [Title] Junctophilin-2 expression silencing causes cardiocyte hypertrophy and abnormal intracellular calcium-handling.
  • Downregulation of JPH2 expression in a model of cardiac hypertrophy was recently associated with defective coupling between plasmalemmal L-type Ca(2+) channels and sarcoplasmic reticular ryanodine receptors.
  • Partial silencing of JPH2 expression in HL-1 cells by a small interfering RNA probe targeted to murine JPH2 mRNA (shJPH2) resulted in myocyte hypertrophy and increased expression of known markers of cardiac hypertrophy.

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  • (PMID = 21216834.001).
  • [ISSN] 1941-3297
  • [Journal-full-title] Circulation. Heart failure
  • [ISO-abbreviation] Circ Heart Fail
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL094291-03; United States / NHLBI NIH HHS / HL / P01-HL94291; United States / NIAMS NIH HHS / AR / R00 AR054793-03; United States / NIAMS NIH HHS / AR / R00 AR054793-04; United States / NICHD NIH HHS / HD / R01 HD042569; United States / NICHD NIH HHS / HD / R01 HD042569-09; United States / NHLBI NIH HHS / HL / R01 HL089598; United States / NHLBI NIH HHS / HL / R01 HL091947; United States / NICHD NIH HHS / HD / R01-HD42569; United States / NHLBI NIH HHS / HL / R01-HL089598; United States / NHLBI NIH HHS / HL / R01-HL091947
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channels, L-Type; 0 / Membrane Proteins; 0 / junctophilin; 3G6A5W338E / Caffeine
  • [Other-IDs] NLM/ NIHMS271398; NLM/ PMC3059380
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32. |......... 1%  Raffaello A, Milan G, Masiero E, Carnio S, Lee D, Lanfranchi G, Goldberg AL, Sandri M: JunB transcription factor maintains skeletal muscle mass and promotes hypertrophy. J Cell Biol; 2010 Oct 4;191(1):101-13
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  • [Title] JunB transcription factor maintains skeletal muscle mass and promotes hypertrophy.
  • Furthermore, JunB overexpression induces hypertrophy without affecting satellite cell proliferation and stimulated protein synthesis independently of the Akt/mTOR pathway.
  • Therefore, JunB is important not only in dividing populations but also in adult muscle, where it is required for the maintenance of muscle size and can induce rapid hypertrophy and block atrophy.
  • [MeSH-minor] Animals. Forkhead Transcription Factors / metabolism. Hypertrophy. Mice. Muscle Fibers, Skeletal / cytology. Muscle Fibers, Skeletal / metabolism. Muscle Proteins / genetics. Muscle Proteins / metabolism. Muscular Atrophy / metabolism. Promoter Regions, Genetic. Protein Biosynthesis. SKP Cullin F-Box Protein Ligases / genetics. SKP Cullin F-Box Protein Ligases / metabolism. Signal Transduction. Ubiquitin-Protein Ligases / metabolism

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  • (PMID = 20921137.001).
  • [ISSN] 1540-8140
  • [Journal-full-title] The Journal of cell biology
  • [ISO-abbreviation] J. Cell Biol.
  • [Language] eng
  • [Grant] Italy / Telethon / / TCR09003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Forkhead Transcription Factors; 0 / FoxO3 protein, mouse; 0 / Muscle Proteins; 0 / Proto-Oncogene Proteins c-jun; EC 6.3.2.19 / Fbxo32 protein, mouse; EC 6.3.2.19 / SKP Cullin F-Box Protein Ligases; EC 6.3.2.19 / Trim63 protein, mouse; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2953439
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33. |......... 1%  Zhang ZY, Liu XH, Hu WC, Rong F, Wu XD: The calcineurin-myocyte enhancer factor 2c pathway mediates cardiac hypertrophy induced by endoplasmic reticulum stress in neonatal rat cardiomyocytes. Am J Physiol Heart Circ Physiol; 2010 May;298(5):H1499-509
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  • [Title] The calcineurin-myocyte enhancer factor 2c pathway mediates cardiac hypertrophy induced by endoplasmic reticulum stress in neonatal rat cardiomyocytes.
  • Our previous study verified that ERS took part in the development of cardiac hypertrophy; however, its mechanism is still unclear.
  • This study aimed to investigate the roles of the calcineurin (CaN) signal pathway in hypertrophy induced by the ERS inductor thapsigargin (TG) in neonatal cardiomyocytes from Sprague-Dawley rats.
  • Investigation of ER chaperone expression, ER staining, and calreticulin immunofluorescence were used to detect the ERS response. mRNA expression of atrial natriuretic peptide and brain natriuretic peptide, total protein synthesis rate, and cell surface area were used to evaluate cardiac hypertrophy induced by TG.
  • TG induced a significant ERS response along with hypertrophy in a dose- and time-dependent manner in cardiomyocytes, which was verified by treatment with tunicamycin, another ERS inducer.
  • Cyclosporine A, a CaN inhibitor, markedly suppressed MEF2c nuclear translocation and inhibited TG-induced hypertrophy.
  • These results demonstrate that ERS induces cardiac hypertrophy and that the CaN-MEF2c pathway is involved in ERS-induced hypertrophy in cardiomyocytes.

  • HSDB. structure - CYCLOSPORIN A.
  • HSDB. structure - CALCIUM, ELEMENTAL.
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  • (PMID = 20207814.001).
  • [ISSN] 1522-1539
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / MEF2 Transcription Factors; 0 / Myogenic Regulatory Factors; 11089-65-9 / Tunicamycin; 63231-63-0 / RNA; 67526-95-8 / Thapsigargin; 83HN0GTJ6D / Cyclosporine; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.1.3.16 / Calcineurin; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium
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34. |......... 1%  Wang KC, Brooks DA, Thornburg KL, Morrison JL: Activation of IGF-2R stimulates cardiomyocyte hypertrophy in the late gestation sheep fetus. J Physiol; 2012 Nov 1;590(Pt 21):5425-37
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  • [Title] Activation of IGF-2R stimulates cardiomyocyte hypertrophy in the late gestation sheep fetus.
  • In vitro studies using rat and fetal sheep cardiomyocytes indicate that, in addition to its role as a clearance receptor, the insulin-like growth factor 2 receptor (IGF-2R) can induce cardiomyocyte hypertrophy.
  • We concluded that infusion of Leu(27)IGF-2 into the left circumflex coronary artery causes cardiac IGF-2R activation in the left ventricle of the heart, and this stimulates cardiomyocyte hypertrophy in a Gαs-dependent manner.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Coronary Vessels. Cyclic AMP-Dependent Protein Kinases / physiology. Fetus. Gestational Age. Hypertrophy. Insulin-Like Growth Factor II / pharmacology. Sheep

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  • (PMID = 22930271.001).
  • [ISSN] 1469-7793
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptor, IGF Type 2; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC3515828
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35. |......... 1%  Waters SB, Diak DM, Zuckermann M, Goldspink PH, Leoni L, Roman BB: Genetic background influences adaptation to cardiac hypertrophy and Ca(2+) handling gene expression. Front Physiol; 2013;4:11
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  • [Title] Genetic background influences adaptation to cardiac hypertrophy and Ca(2+) handling gene expression.
  • Genetic variability has a profound effect on the development of cardiac hypertrophy in response to stress.
  • Metabolically, the brain isoform of creatine kinase (Ckb) was up-regulated in response to ISO in C57BL/6J but not in 129/SvJ.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 23508205.001).
  • [ISSN] 1664-042X
  • [Journal-full-title] Frontiers in physiology
  • [ISO-abbreviation] Front Physiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3589715
  • [Keywords] NOTNLM ; Ca2+-handling / gene expression / heart / hemodynamics / hypertrophy / mouse
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36. |......... 1%  Usher MG, Duan SZ, Ivaschenko CY, Frieler RA, Berger S, Schütz G, Lumeng CN, Mortensen RM: Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice. J Clin Invest; 2010 Sep;120(9):3350-64
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  • [Title] Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice.
  • In vivo, MR deficiency in macrophages mimicked the effects of MR antagonists and protected against cardiac hypertrophy, fibrosis, and vascular damage caused by L-NAME/Ang II.
  • [MeSH-minor] Aldosterone / blood. Aldosterone / pharmacology. Animals. Blood Pressure / drug effects. Blood Pressure / physiology. Cardiomegaly / pathology. Cardiovascular Diseases / pathology. Fibrosis / pathology. Heart / drug effects. Heart / physiopathology. Hypertension / pathology. Hypertension / physiopathology. Hypertrophy / pathology. Interleukin-4 / pharmacology. Macrophages / drug effects. Mice. Mice, Knockout. Mice, Transgenic. NG-Nitroarginine Methyl Ester / pharmacology. Receptors, Glucocorticoid / antagonists & inhibitors. Receptors, Glucocorticoid / physiology

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  • (PMID = 20697155.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE23308
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK078851-05; United States / NHLBI NIH HHS / HL / R01HL083201
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 0 / NR3C1 protein, human; 0 / Receptors, Glucocorticoid; 0 / Receptors, Mineralocorticoid; 207137-56-2 / Interleukin-4; 4964P6T9RB / Aldosterone; V55S2QJN2X / NG-Nitroarginine Methyl Ester
  • [Other-IDs] NLM/ PMC2929712
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37. |......... 1%  Schuman ML, Landa MS, Toblli JE, Peres Diaz LS, Alvarez AL, Finkielman S, Paz L, Cao G, Pirola CJ, García SI: Cardiac thyrotropin-releasing hormone mediates left ventricular hypertrophy in spontaneously hypertensive rats. Hypertension; 2011 Jan;57(1):103-9
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  • [Title] Cardiac thyrotropin-releasing hormone mediates left ventricular hypertrophy in spontaneously hypertensive rats.
  • Local thyrotropin-releasing hormone (TRH) may be involved in cardiac pathophysiology, but its role in left ventricular hypertrophy (LVH) is still unknown.
  • We studied whether local TRH is involved in LVH of spontaneously hypertensive rats (SHR) by investigating TRH expression and its long-term inhibition by interference RNA (TRH-iRNA) during LVH development at 2 stages (prehypertrophy and hypertrophy).
  • Cardiac hypertrophy was expressed as heart/total body weight (HW/BW) ratio.
  • TRH content (radioimmuno assay), preproTRH, TRH receptor type I, brain natriuretic peptide (BNP), and collagen mRNA expressions (real-time polymerase chain reaction) were measured.
  • [MeSH-major] Hypertrophy, Left Ventricular / metabolism. Thyrotropin-Releasing Hormone / metabolism
  • [MeSH-minor] Actins / analysis. Animals. Collagen Type III / analysis. Male. Natriuretic Peptide, Brain / analysis. RNA Interference. Rats. Rats, Inbred SHR. Rats, Inbred WKY. Receptors, Thyrotropin-Releasing Hormone / analysis

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  • [CommentIn] Hypertension. 2011 Jan;57(1):26-8 [21135355.001]
  • (PMID = 21135357.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Collagen Type III; 0 / Receptors, Thyrotropin-Releasing Hormone; 0 / TRH-receptor-1, rat; 0 / smooth muscle actin, rat; 114471-18-0 / Natriuretic Peptide, Brain; 5Y5F15120W / Thyrotropin-Releasing Hormone
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38. |......... 1%  Lin PP, Hsieh YM, Kuo WW, Lin CC, Tsai FJ, Tsai CH, Huang CY, Tsai CC: Inhibition of cardiac hypertrophy by probiotic-fermented purple sweet potato yogurt in spontaneously hypertensive rat hearts. Int J Mol Med; 2012 Dec;30(6):1365-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of cardiac hypertrophy by probiotic-fermented purple sweet potato yogurt in spontaneously hypertensive rat hearts.
  • Cardiovascular hypertrophy is a common feature of hypertension and an important risk factor for heart damage.
  • The regression of cardiovascular hypertrophy is currently considered an important therapeutic target in reducing the omplications of hypertension.
  • The aim of this study was to investigate the inhibition of cardiac hypertrophy by probiotic-fermented purple sweet potato yogurt (PSPY) with high γ-aminobutyric acid (GABA) content in spontaneously hypertensive rat (SHR) hearts.
  • The changes in myocardial architecture and key molecules of the hypertrophy-related pathway in the excised left ventricle from these rats were determined by histopathological analysis, hematoxylin and eosin staining and western blot analysis.
  • Moreover, the increases in atrial natriuretic peptide, B-type natriuretic peptide, phosphorilated protein kinase Cα and calmodulin-dependent protein kinase II levels in the left ventricle were accompanied by hypertension and increases in phosphorylated extracellular signal-regulated kinase 5 activities with enhanced cardiac hypertrophy.
  • PSPY may repress the activation of ANP and BNP which subsequently inhibit the dephosphorylation of the nuclear factor of activated T-cells, cytoplasmic 3 and ultimately prevent the progression of cardiac hypertrophy.
  • [MeSH-major] Antihypertensive Agents / administration & dosage. Hypertension / diet therapy. Hypertrophy, Left Ventricular / prevention & control. Ipomoea batatas / chemistry. Yogurt
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / metabolism. Calcineurin / metabolism. Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism. Captopril / administration & dosage. Heart Ventricles / drug effects. Heart Ventricles / metabolism. Heart Ventricles / pathology. Insulin-Like Growth Factor II / metabolism. Interleukin-6 / metabolism. Male. Mitogen-Activated Protein Kinase 7 / metabolism. NFATC Transcription Factors / metabolism. Natriuretic Peptide, Brain / metabolism. Organ Size. Protein Kinase C-alpha / metabolism. Rats. Rats, Inbred SHR. Rats, Inbred WKY. gamma-Aminobutyric Acid / administration & dosage

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  • (PMID = 23064753.001).
  • [ISSN] 1791-244X
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Interleukin-6; 0 / NFATC Transcription Factors; 114471-18-0 / Natriuretic Peptide, Brain; 56-12-2 / gamma-Aminobutyric Acid; 67763-97-7 / Insulin-Like Growth Factor II; 85637-73-6 / Atrial Natriuretic Factor; 9G64RSX1XD / Captopril; EC 2.7.11.13 / Protein Kinase C-alpha; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 7; EC 3.1.3.16 / Calcineurin
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39. |......... 1%  Yang JH, Ma CG, Cai Y, Pan CS, Zhao J, Tang CS, Qi YF: Effect of intermedin1-53 on angiotensin II-induced hypertrophy in neonatal rat ventricular myocytes. J Cardiovasc Pharmacol; 2010 Jul;56(1):45-52
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  • [Title] Effect of intermedin1-53 on angiotensin II-induced hypertrophy in neonatal rat ventricular myocytes.
  • The present study was designed to observe the interaction between IMD and cardiac hypertrophy and the possible mechanism involved in the antihypertrophic effects of IMD1-53 in cultured neonatal ventricular myocytes.
  • METHODS: Myocyte hypertrophy was induced by treating the cells with angiotensin II, and the hypertrophic response was characterized by a significant increase in cell surface area, protein synthesis, and BNP mRNA expression.
  • CONCLUSIONS: Thus, IMD and its receptor system are involved in cardiac hypertrophy, and like adrenomedullin, IMD1-53 exerts an antihypertrophic effect on neonatal cardiomyocytes and the effect can be mediated by the cAMP/PKA pathway.
  • [MeSH-minor] Angiotensin II / toxicity. Animals. Animals, Newborn. Cells, Cultured. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Heart Ventricles / cytology. Heart Ventricles / physiopathology. Natriuretic Peptide, Brain / genetics. RNA, Messenger / metabolism. Rats. Rats, Wistar

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  • (PMID = 20351561.001).
  • [ISSN] 1533-4023
  • [Journal-full-title] Journal of cardiovascular pharmacology
  • [ISO-abbreviation] J. Cardiovasc. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuropeptides; 0 / RNA, Messenger; 0 / intermedin protein, rat; 11128-99-7 / Angiotensin II; 114471-18-0 / Natriuretic Peptide, Brain; 148498-78-6 / Adrenomedullin; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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40. |......... 1%  Zhang Y, Cao Y, Duan H, Wang H, He L: Imperatorin prevents cardiac hypertrophy and the transition to heart failure via NO-dependent mechanisms in mice. Fitoterapia; 2012 Jan;83(1):60-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imperatorin prevents cardiac hypertrophy and the transition to heart failure via NO-dependent mechanisms in mice.
  • Augmented endothelial nitric oxide (NO) synthase (eNOS) signaling has been reported to be associated with improvements in cardiac remodeling, and NO levels have been shown to be related to cardiac hypertrophy and heart failure.
  • Imperatorin, a dietary furanocoumarin, has been shown to prevent cardiac hypertrophy in the spontaneous hypertension rats (SHR).
  • Thus, we aimed to clarify whether imperatorin attenuates both cardiac hypertrophy and heart failure via the NO-signaling pathway.
  • Imperatorin can attenuate cardiac hypertrophy both in vivo and in vitro, and halt the process leading from hypertrophy to heart failure by a NO-mediated pathway.
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / genetics. Atrial Natriuretic Factor / metabolism. Cells, Cultured. Cytoplasmic Dyneins / genetics. Cytoplasmic Dyneins / metabolism. Gene Expression Regulation / drug effects. Male. Mice. Myocytes, Cardiac / drug effects. Myocytes, Cardiac / metabolism. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism. Nitric Oxide Synthase Type III / genetics. Nitric Oxide Synthase Type III / metabolism. Rats. Sarcoplasmic Reticulum Calcium-Transporting ATPases / genetics. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism

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  • [Copyright] Copyright © 2011 Elsevier B.V. All rights reserved.
  • (PMID = 21983344.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Psoralens; 114471-18-0 / Natriuretic Peptide, Brain; 31C4KY9ESH / Nitric Oxide; 85637-73-6 / Atrial Natriuretic Factor; EC 1.14.13.39 / Nitric Oxide Synthase Type III; EC 3.6.1.- / Dynll1 protein, rat; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.4.2 / Cytoplasmic Dyneins; K713N25C78 / imperatorin
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41. |......... 1%  Lv R, Zhang C, Liu Y, Gu YP, Huang W, Guo W, Wei HC, Chen LY: [Dynamic study on inhibition of qi-benefiting, blood-activating recipe on myocardial hypertrophy induced by ISO in rats]. Zhong Yao Cai; 2010 May;33(5):749-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Dynamic study on inhibition of qi-benefiting, blood-activating recipe on myocardial hypertrophy induced by ISO in rats].
  • OBJECTIVE: To observe the effect of Qi-Benefiting, Blood-Activating Recipe on the different pathologic stage of myocardial hypertrophy induced by ISO in rats.
  • METHODS: Myocardial hypertrophy rats were induced by isoproterenol, and treated with Qi-Benefiting, Blood-Activating Recipe for 5,10 and 15 weeks, hemodynamic parameters, LVMI, HMI were determined, ANP and BNP were analysed.
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / blood. Drug Combinations. Isoproterenol / administration & dosage. Male. Myocardium / pathology. Natriuretic Peptide, Brain / blood. Plants, Medicinal / chemistry. Qi. Random Allocation. Rats. Rats, Sprague-Dawley

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  • (PMID = 20873559.001).
  • [ISSN] 1001-4454
  • [Journal-full-title] Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials
  • [ISO-abbreviation] Zhong Yao Cai
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 114471-18-0 / Natriuretic Peptide, Brain; 85637-73-6 / Atrial Natriuretic Factor; L628TT009W / Isoproterenol
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42. |......... 1%  Yamazaki T, Yamashita N, Izumi Y, Nakamura Y, Shiota M, Hanatani A, Shimada K, Muro T, Iwao H, Yoshiyama M: The antifibrotic agent pirfenidone inhibits angiotensin II-induced cardiac hypertrophy in mice. Hypertens Res; 2012 Jan;35(1):34-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The antifibrotic agent pirfenidone inhibits angiotensin II-induced cardiac hypertrophy in mice.
  • Therefore, we investigated whether pirfenidone has a potential role in preventing angiotensin II (Ang II)-induced cardiac hypertrophy.
  • Echocardiography revealed that left ventricular hypertrophy was significantly increased in the vehicle group vs. the control group.
  • Pirfenidone also inhibited Ang II-induced hypertrophy.
  • In the vehicle group, the mRNA expressions of atrial natriuretic peptide, brain natriuretic peptide and transforming growth factor-β1 were increased, which was significantly inhibited by pirfenidone.
  • These results indicate that pirfenidone might be effective as an antifibrotic drug in the treatment of cardiac hypertrophy induced by hypertension.

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  • (PMID = 21866107.001).
  • [ISSN] 1348-4214
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pyridones; 11128-99-7 / Angiotensin II; D7NLD2JX7U / pirfenidone
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43. |......... 1%  Yang J, Zhu HH, Chen GP, Ye Y, Zhao CZ, Mou Y, Hu SJ: Inhibition of farnesyl pyrophosphate synthase attenuates angiotensin II-induced cardiac hypertrophy and fibrosis in vivo. Int J Biochem Cell Biol; 2013 Mar;45(3):657-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of farnesyl pyrophosphate synthase attenuates angiotensin II-induced cardiac hypertrophy and fibrosis in vivo.
  • We have previously demonstrated that both knockdown of FPPS with small interfering RNA and inhibition of FPPS by alendronate could prevent Ang II-induced hypertrophy in cultured cardiomyocytes.
  • In this study, we evaluated the effects of FPPS inhibition in Ang II-mediated cardiac hypertrophy and fibrosis in vivo.
  • In the meantime, FPPS inhibition attenuated Ang II-mediated cardiac hypertrophy and fibrosis as indexed by the heart weight to body weight ratio, echocardiographic parameters, histological examinations and expression of ANP and BNP mRNA.
  • In conclusion, FPPS might play an important role in Ang II-induced cardiac hypertrophy and fibrosis in vivo, at least in part through RhoA, p-38 MAPK and TGF-β1.
  • [MeSH-minor] Alendronate / pharmacology. Animals. Atrial Natriuretic Factor / metabolism. Gene Expression Regulation. Humans. Male. Mice. Myocytes, Cardiac / metabolism. Myocytes, Cardiac / pathology. Natriuretic Peptide, Brain / contraindications. Natriuretic Peptide, Brain / metabolism. Signal Transduction. Terpenes / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [Copyright] Copyright © 2012 Elsevier Ltd. All rights reserved.
  • (PMID = 23277274.001).
  • [ISSN] 1878-5875
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Terpenes; 0 / Transforming Growth Factor beta1; 11128-99-7 / Angiotensin II; 114471-18-0 / Natriuretic Peptide, Brain; 85637-73-6 / Atrial Natriuretic Factor; EC 2.5.1.10 / Geranyltranstransferase; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.6.5.2 / RhoA protein, mouse; EC 3.6.5.2 / rho GTP-Binding Proteins; X1J18R4W8P / Alendronate
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44. |......... 1%  Horton JS, Buckley CL, Stokes AJ: Successful TRPV1 antagonist treatment for cardiac hypertrophy and heart failure in mice. Channels (Austin); 2013 Jan 1;7(1):17-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful TRPV1 antagonist treatment for cardiac hypertrophy and heart failure in mice.
  • In a pre-clinical model of cardiac hypertrophy and heart failure, we were able to overcome loss of heart function by administering the TRPV1 antagonist BCTC (4-(3-Chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide).
  • The results presented here identify TRPV1 antagonists as new treatment options for cardiac hypertrophy and heart failure.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Disease Models, Animal. Humans. Male. Matrix Metalloproteinase 9 / genetics. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred C57BL. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism

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  • (PMID = 23221478.001).
  • [ISSN] 1933-6969
  • [Journal-full-title] Channels (Austin, Tex.)
  • [ISO-abbreviation] Channels (Austin)
  • [Language] eng
  • [Grant] United States / NIMHD NIH HHS / MD / P20 MD006084; United States / NIMHD NIH HHS / MD / P20MD006084; United States / NCRR NIH HHS / RR / P20RR016467; United States / NIMHD NIH HHS / MD / U54 MD007584; United States / NIMHD NIH HHS / MD / U54MD007584
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)tetrahydropyrazine-1(2H)-carboxamide; 0 / Pyrazines; 0 / Pyridines; 0 / TRPV Cation Channels; 0 / TRPV1 protein, mouse; 114471-18-0 / Natriuretic Peptide, Brain; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC3589277
  • [Keywords] NOTNLM ; TRPV1 / apoptosis / cardiac hypertrophy / fibrosis / heart failure / pressure overload
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45. |......... 1%  Zhang J, Zhang BH, Yu YR, Tang CS, Qi YF: Adrenomedullin protects against fructose-induced insulin resistance and myocardial hypertrophy in rats. Peptides; 2011 Jul;32(7):1415-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenomedullin protects against fructose-induced insulin resistance and myocardial hypertrophy in rats.
  • mRNA level and content of brain natriuretic peptide (BNP) in myocardial were all increased significantly.
  • ADM administration ameliorated the induced IR and myocardial hypertrophy.
  • Our results showed upregulation of endogenous ADM during fructose-induced IR and the protective effect of ADM on fructose-induced IR and concomitant cardiovascular hypertrophy probably by its antioxidant effect, which suggests that ADM could be an endogenous protective factor in IR.
  • [MeSH-major] Adrenomedullin. Cardiomegaly / blood. Cardiotonic Agents. Fructose / adverse effects. Insulin Resistance. Myocardium / metabolism. Natriuretic Peptide, Brain / biosynthesis

  • HSDB. structure - MALONALDEHYDE.
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  • [Copyright] Copyright © 2011 Elsevier Inc. All rights reserved.
  • (PMID = 21664393.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Cardiotonic Agents; 0 / Insulin; 0 / RNA, Messenger; 114471-18-0 / Natriuretic Peptide, Brain; 148498-78-6 / Adrenomedullin; 30237-26-4 / Fructose; 4Y8F71G49Q / Malondialdehyde; 9005-79-2 / Glycogen
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46. |......... 1%  Li J, Liao Y, Lu L, Lu L, Feng J, Wu W, Liu X: [Preliminary investigation into the mechanism of cardiomyocyte hypertrophy induced by visfatin]. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi; 2014 Apr;31(2):379-84
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  • [Title] [Preliminary investigation into the mechanism of cardiomyocyte hypertrophy induced by visfatin].
  • The aim of the current study is to investigate the effect of visfatin on cardiomyocyte hypertrophy.
  • Cultured H9c2 cardiomyocytes were exposed to visfatin at different concentrations for different periods of time, and the markers of cardiomyocyte hypertrophy were detected.
  • The mRNA expressions of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and ERS markers including glucose-regulated protein 78(GRP78), C/EPB homologous protein (CHOP) and activating transcription factor 6 (ATF6) were assessed by real time RT-PCR.
  • The experimental data demonstrated that exposure to 100 or 150 ng/mL concentrations of visfatin for 24 h, or 100 ng/mL of visfatin for 24 or 48 h, significantly increased the expression of markers for cardiomyocyte hypertrophy.
  • Furthermore, pre-treatment with pravastatin partially inhibited the visfatin-induced mRNA expression of ANP and BNP in H9c2 cells, whereas thapsigargin promoted the visfatin-induced expression of cardiomyocyte hypertrophy markers.
  • The results suggest that visfatin might induce cardiomyocyte hypertrophy via ERS -dependent pathways.

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  • (PMID = 25039146.001).
  • [ISSN] 1001-5515
  • [Journal-full-title] Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi
  • [ISO-abbreviation] Sheng Wu Yi Xue Gong Cheng Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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47. |......... 1%  Patterson C, Portbury AL, Schisler JC, Willis MS: Tear me down: role of calpain in the development of cardiac ventricular hypertrophy. Circ Res; 2011 Aug 5;109(4):453-62
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  • [Title] Tear me down: role of calpain in the development of cardiac ventricular hypertrophy.
  • Cardiac hypertrophy develops most commonly in response to hypertension and is an independent risk factor for the development of heart failure.
  • The mechanisms by which cardiac hypertrophy may be reversed to reduce this risk have not been fully determined to the point where mechanism-specific therapies have been developed.
  • Recently, proteases in the calpain family have been implicated in the regulation of the development of cardiac hypertrophy in preclinical animal models.
  • In this review, we summarize the molecular mechanisms by which calpain inhibition has been shown to modulate the development of cardiac (specifically ventricular) hypertrophy.
  • The context within which calpain inhibition might be developed for therapeutic intervention of cardiac hypertrophy is then discussed.

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  • (PMID = 21817165.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM061728; United States / NIGMS NIH HHS / GM / R01 GM061728-10; United States / NHLBI NIH HHS / HL / R01 HL104129; United States / NHLBI NIH HHS / HL / R01 HL104129-01; United States / NHLBI NIH HHS / HL / R01HL065619; United States / NHLBI NIH HHS / HL / R01HL104129; United States / NHLBI NIH HHS / HL / R37 HL065619-12; United States / NHLBI NIH HHS / HL / T32 HL083828
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cardiovascular Agents; 0 / Cysteine Proteinase Inhibitors; EC 3.4.22.- / Calpain
  • [Other-IDs] NLM/ NIHMS303111; NLM/ PMC3151485
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48. |......... 1%  Kiso H, Ohba T, Iino K, Sato K, Terata Y, Murakami M, Ono K, Watanabe H, Ito H: Sildenafil prevents the up-regulation of transient receptor potential canonical channels in the development of cardiomyocyte hypertrophy. Biochem Biophys Res Commun; 2013 Jul 5;436(3):514-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sildenafil prevents the up-regulation of transient receptor potential canonical channels in the development of cardiomyocyte hypertrophy.
  • BACKGROUND: Transient receptor potential canonical (TRPCs) channels are up-regulated in the development of cardiac hypertrophy.
  • Sildenafil inhibits TRPC6 activation and expression, leading to the prevention of cardiac hypertrophy.
  • We hypothesized that in addition to its effects of TRPC6, sildenafil blocks the up-regulation of other TRPC channels to suppress cardiomyocyte hypertrophy.
  • METHODS AND RESULTS: In cultured neonatal rat cardiomyocytes, a 48 h treatment with 10nM endothelin (ET)-1 induced hypertrophic responses characterized by nuclear factor of activated T cells activation and enhancement of brain natriuretic peptide expression and cell surface area.
  • CONCLUSIONS: These results suggest that sildenafil inhibits cardiomyocyte hypertrophy by suppressing the up-regulation of TRPC expression.

  • HSDB. structure - CALCIUM, ELEMENTAL.
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  • [Copyright] Copyright © 2013 Elsevier Inc. All rights reserved.
  • (PMID = 23764398.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / NFATC Transcription Factors; 0 / Piperazines; 0 / Purines; 0 / Sulfones; 0 / TRPC Cation Channels; 0 / TRPC3 cation channel; 0 / transient receptor potential cation channel, subfamily C, member 1; 3M7OB98Y7H / sildenafil; SY7Q814VUP / Calcium
  • [Keywords] NOTNLM ; Ca(2+) entry / Cardiomyocyte hypertrophy / Sildenafil / TRPC channels
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49. |......... 1%  He T, Chen L, Chen Y, Han Y, Yang WQ, Jin MW: In vivo and in vitro protective effects of pentamethylquercetin on cardiac hypertrophy. Cardiovasc Drugs Ther; 2012 Apr;26(2):109-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo and in vitro protective effects of pentamethylquercetin on cardiac hypertrophy.
  • AIM: To investigate the in vivo and in vitro protective effects of pentamethylquercetin (PMQ), a member of polymethoxy flavonoids (PMFs), on cardiac hypertrophy.
  • METHODS: An in vivo cardiac hypertrophy model established by abdominal aorta banding technique in rats was treated with PMQ in increasing dosages (2.5, 5, and 10 mg x kg(-1) x d(-1)).
  • An in vitro cardiomyocyte hypertrophy model was induced by treating neonatal cardiomyocytes with endothelin-1 (ET-1, 0.1 μM).
  • The resultant cardiac hypertrophy and heart failure were characterized by a significant increase in the heart and lung indices (3.51 ± 0.30 vs 2.35 ± 0.24, 5.58 ± 0.85 vs 3.94 ± 0.54; both P < 0.01), cardiomyocyte cross-sectional areas (153 ± 33% vs 100 ± 5%, P < 0.01) and myocardial fibrosis (9.09 ± 1.30% vs 1.49 ± 0.20%, P < 0.01) with concomitant elevation of B-type natriuretic peptide and cardiac collagen mRNA level.
  • CONCLUSION: PMQ has significant protective effects on cardiac hypertrophy through up-regulating the mRNA and protein levels of PPAR α and PPAR β involved in the process of inflammation response and cardiac fibrosis.
  • [MeSH-minor] Aldosterone / adverse effects. Animals. Blood Pressure / drug effects. Cells, Cultured. Collagen / metabolism. Down-Regulation / drug effects. Endothelin-1. Fibroblasts / drug effects. Fibroblasts / metabolism. Fibroblasts / pathology. Fibrosis / chemically induced. Fibrosis / drug therapy. Fibrosis / metabolism. Fibrosis / pathology. Heart Failure / drug therapy. Heart Failure / metabolism. Heart Failure / pathology. Hemodynamics / drug effects. Interleukin-6 / metabolism. Male. Natriuretic Peptide, Brain / metabolism. PPAR alpha / metabolism. PPAR-beta / metabolism. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation / drug effects

  • HSDB. structure - QUERCETIN.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 22183794.001).
  • [ISSN] 1573-7241
  • [Journal-full-title] Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy
  • [ISO-abbreviation] Cardiovasc Drugs Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3,3',4',5,7-pentamethylquercetin; 0 / Cardiotonic Agents; 0 / Endothelin-1; 0 / Interleukin-6; 0 / PPAR alpha; 0 / PPAR-beta; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 114471-18-0 / Natriuretic Peptide, Brain; 4964P6T9RB / Aldosterone; 9007-34-5 / Collagen; 9IKM0I5T1E / Quercetin
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50. |......... 1%  Ehrentraut H, Weber C, Ehrentraut S, Schwederski M, Boehm O, Knuefermann P, Meyer R, Baumgarten G: The toll-like receptor 4-antagonist eritoran reduces murine cardiac hypertrophy. Eur J Heart Fail; 2011 Jun;13(6):602-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The toll-like receptor 4-antagonist eritoran reduces murine cardiac hypertrophy.
  • Deficiency of TLR4 attenuates the development of left ventricular hypertrophy after transverse aortic constriction (TAC) in mice.
  • We hypothesized that application of the TLR4 antagonist eritoran may also reduce cardiac hypertrophy after TAC surgery.
  • CONCLUSION: Application of the TLR4 antagonist eritoran attenuates the development of cardiac hypertrophy possibly by a reduction in inflammatory and increase in anti-inflammatory cytokines.
  • [MeSH-minor] Animals. Disease Models, Animal. Electrophoresis, Polyacrylamide Gel. Enzyme-Linked Immunosorbent Assay. Interleukins / metabolism. Male. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred C57BL. Natriuretic Peptide, Brain / metabolism. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 21613426.001).
  • [ISSN] 1879-0844
  • [Journal-full-title] European journal of heart failure
  • [ISO-abbreviation] Eur. J. Heart Fail.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Disaccharides; 0 / Interleukins; 0 / Sugar Phosphates; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 4; 114471-18-0 / Natriuretic Peptide, Brain; 551541VI0Y / eritoran; EC 3.4.24.35 / Matrix Metalloproteinase 9
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