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1. Biomedical articles (top 50; 2010 to 2015)
1. 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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  • 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.

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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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2. 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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  • 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; 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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3. 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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  • [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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4. 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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  • [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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5. Blaauw E, van Nieuwenhoven FA, Willemsen P, Delhaas T, Prinzen FW, Snoeckx LH, van Bilsen M, van der Vusse GJ: Stretch-induced hypertrophy of isolated adult rabbit cardiomyocytes. Am J Physiol Heart Circ Physiol; 2010 Sep;299(3):H780-7
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  • [Title] Stretch-induced hypertrophy of isolated adult rabbit cardiomyocytes.
  • The aim of the present study was to investigate whether cyclic equibiaxial stretch is a direct stimulus for isolated adult rabbit cardiomyocytes to develop hypertrophy and to explore the potential involvement of the autocrine/paracrine factors ANG II, transforming growth factor (TGF)-beta(1), and IGF-I in this process.
  • Cyclic stretch significantly increased cell surface area (+3.1%), protein synthesis (+21%), and brain natriuretic peptide (BNP) mRNA expression (6-fold) in cardiomyocytes.
  • This study clearly indicates that cyclic stretch is a strong, direct trigger to induce hypertrophy in fully differentiated rabbit cardiomyocytes.
  • The present findings do not support the notion that stretch-mediated hypertrophy of adult rabbit cardiomyocytes involves autocrine/paracrine actions of ANG II, TGF-beta(1), or IGF-I.
  • [MeSH-minor] Angiotensin II / genetics. Angiotensin II / metabolism. Angiotensin II / pharmacology. Animals. Cell Size. Cells, Cultured. Culture Media, Conditioned. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / metabolism. Insulin-Like Growth Factor I / pharmacology. Male. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rabbits. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / pharmacology

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  • (PMID = 20639217.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 11128-99-7 / Angiotensin II; 114471-18-0 / Natriuretic Peptide, Brain; 67763-96-6 / Insulin-Like Growth Factor I
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6. He Q: Tafazzin knockdown causes hypertrophy of neonatal ventricular myocytes. Am J Physiol Heart Circ Physiol; 2010 Jul;299(1):H210-6
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  • [Title] Tafazzin knockdown causes hypertrophy of neonatal ventricular myocytes.
  • When we tested whether tafazzin knockdown causes hypertrophy in vitro, we found that the surface area of NVMs infected with tafazzin shRNA adenovirus was significantly increased, as were the protein synthesis and expression of the hypertrophic marker gene, brain natriuretic peptide.
  • Taken together, our data support the concept that a decreased tafazzin expression causes cardiomyocyte hypertrophy in vitro.
  • [MeSH-minor] AMP-Activated Protein Kinases / metabolism. Adenosine Triphosphate / metabolism. Adenoviridae / genetics. Animals. Animals, Newborn. Cardiolipins / metabolism. Cells, Cultured. Energy Metabolism. Gene Knockdown Techniques. Genetic Vectors. Heart Ventricles / metabolism. Heart Ventricles / pathology. Mitochondria, Heart / metabolism. Natriuretic Peptide, Brain / metabolism. Phosphorylation. RNA Interference. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Transfection

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  • (PMID = 20348225.001).
  • [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 / Cardiolipins; 0 / RNA, Messenger; 0 / TAZ protein, rat; 0 / Transcription Factors; 114471-18-0 / Natriuretic Peptide, Brain; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.11.1 / AMP-Activated Protein Kinases
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7. Chowdhury R, Nimmanapalli R, Graham T, Reddy G: Curcumin attenuation of lipopolysaccharide induced cardiac hypertrophy in rodents. ISRN Inflamm; 2013;2013:539305
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  • [Title] Curcumin attenuation of lipopolysaccharide induced cardiac hypertrophy in rodents.
  • To study the ameliorating effects of curcumin in lipopolysaccharide (LPS) induced cardiac hypertrophy, mice were assigned to 4 groups (3 males and 3 females in each group): (A) control, (B) curcumin: 100  μ g/kg of body weight by intraperitoneal route (IP), (C) LPS: 60 mg/kg (IP), and (D) LPS + curcumin: both at previously stated concentrations by IP route.
  • The hearts were collected, photographed for cardiomegaly, and weighed to compare heart weight/brain weight (HW/BW) in mg/mg.

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  • (PMID = 24236240.001).
  • [ISSN] 2090-8695
  • [Journal-full-title] ISRN inflammation
  • [ISO-abbreviation] ISRN Inflamm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3819047
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8. Cooper IF, Siadaty MS: 'Hormones' associated with 'Brain Hypertrophy': Top Publications. BioMedLib Review; Hormone;BrainHypertrophy:705185003. ISSN: 2331-5717. 2014/4/22
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  • [Title] 'Hormones' associated with 'Brain Hypertrophy': Top Publications.
  • [Transliterated title]
  • Background: There are articles published each month which present 'Hormone' for 'brain hypertrophy'.
  • Finding such articles is important for researchers, clinicians, and patients.
  • However these articles are spread across thousands of journals, and there are many types of 'Hormone'.
  • This makes searching and locating the relevant publications a challenge.
  • We have used BioMedLib's semantic search technology to address the issue, and gathered all the pertinent publications in this review article.
  • Methods: We categorized the publications we found into two groups.
  • We used the strength of textual-association to separate the groups.
  • In group one there are publications with the strongest evidence of association. We focused finding the most relevant publications pertinent to our goal, rather than combining them into a conclusion section. Such textual synthesis will be the focus of our next project.
  • Results: Group one includes 17 publications, and group two 3890 publications.
  • Here are the top 10.
  • Green PH: On Hypertrophy of the Brain in Children.
  • Lees C: Observations on Hypertrophy of the Brain in Children.
  • 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.
  • Nakagawa O et al: Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an "emergency" cardiac hormone against ventricular overload.
  • Mouly-Bertin C et al: N-terminal pro-brain natriuretic peptide--a promising biomarker for the diagnosis of left ventricular hypertrophy in hypertensive women.
  • Sims J: On Hypertrophy and Atrophy of the Brain.
  • Donahue LR et al: Megencephaly: a new mouse mutation on chromosome 6 that causes hypertrophy of the brain.
  • Kawakami H et al: Alteration of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats.
  • Cho HJ et al: Hypertrophy of the vasa vasorum: vascular response to the hungry brain.
  • Murakami Y et al: New insights into the mechanism of the elevation of plasma brain natriuretic polypeptide levels in patients with left ventricular hypertrophy.

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 705185003.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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9. Cooper IF, Siadaty MS: 'Pharmacologic Substances' associated with 'Brain Hypertrophy': Top Publications. BioMedLib Review; PharmacologicSubstance;BrainHypertrophy:706260401. ISSN: 2331-5717. 2014/10/24
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  • [Title] 'Pharmacologic Substances' associated with 'Brain Hypertrophy': Top Publications.
  • [Transliterated title]
  • Background: There are articles published each month which present 'Pharmacologic Substance' for 'brain hypertrophy'.
  • Finding such articles is important for researchers, clinicians, and patients.
  • However these articles are spread across thousands of journals, and there are many types of 'Pharmacologic Substance'.
  • This makes searching and locating the relevant publications a challenge.
  • We have used BioMedLib's semantic search technology to address the issue, and gathered all the pertinent publications in this review article.
  • Methods: We categorized the publications we found into two groups.
  • We used the strength of textual-association to separate the groups.
  • In group one there are publications with the strongest evidence of association. We focused finding the most relevant publications pertinent to our goal, rather than combining them into a conclusion section. Such textual synthesis will be the focus of our next project.
  • Results: Group one includes 23 publications, and group two 2738 publications.
  • Here are the top 10.
  • Cooper IF et al: 'Amino Acids, Peptides, or Proteins' associated with 'Brain Hypertrophy': Top Publications.
  • 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.
  • Campos LA et al: Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen.
  • Baltatu O et al: The brain renin-angiotensin system modulates angiotensin II-induced hypertension and cardiac 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.
  • Elliott MB et al: Hypertonic saline attenuates tissue loss and astrocyte hypertrophy in a model of traumatic brain injury.
  • Murakami Y et al: New insights into the mechanism of the elevation of plasma brain natriuretic polypeptide levels in patients with left ventricular hypertrophy.
  • 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.
  • Katz E et al: T4-induced cardiac hypertrophy disrupts cyclic GMP mediated responses to brain natriuretic peptide in rabbit myocardium.

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 706260401.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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10. Santos AC, Escorsi-Rosset S, Simao GN, Terra VC, Velasco T, Neder L, Sakamoto AC, Machado HR: Hemispheric dysplasia and hemimegalencephaly: imaging definitions. Childs Nerv Syst; 2014 Nov;30(11):1813-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND AND PURPOSE: Hemispheric dysplasia (HD) and hemimegalencephaly (HME) are both brain malformations with early clinical manifestation including developmental delay and intractable epilepsy.
  • On the other hand, HD shows no brain hypertrophy, and even brain atrophy, eventually.
  • The combination of WM dysmyelination and hypertrophy leads to the so called hamartomatous appearing.
  • Although not all HME showed brain enlargement and some HD might show no size changes or atrophy, the size of affected hemisphere and the hamartomatous appearance of the WM were the more relevant signs to differentiate both conditions.
  • CONCLUSION: Brain MRI was the best diagnostic tolls because it allowed together high contrast resolution, whole brain coverage and spatial distribution analysis.
  • HD and HMD showed brain asymmetry tendency, but in opposite directions.

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  • (PMID = 25296542.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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11. 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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12. 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] 2331-2637
  • [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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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. 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.
  • [Transliterated title]
  • Background: There are articles published each month which present 'amino acid peptide or protein' for 'brain hypertrophy'.
  • Finding such articles is important for researchers, clinicians, and patients.
  • However these articles are spread across thousands of journals, and there are many types of 'amino acid peptide or protein'.
  • This makes searching and locating the relevant publications a challenge.
  • We have used BioMedLib's semantic search technology to address the issue, and gathered all the pertinent publications in this review article.
  • Methods: We categorized the publications we found into two groups.
  • We used the strength of textual-association to separate the groups.
  • In group one there are publications with the strongest evidence of association. We focused finding the most relevant publications pertinent to our goal, rather than combining them into a conclusion section. Such textual synthesis will be the focus of our next project.
  • Results: Group one includes 20 publications, and group two 2158 publications.
  • Here are the top 10.
  • 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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15. Cooper IF, Siadaty MS: 'Body PartsCMMA OrgansCMMA or Organ Components' associated with 'Pyloric Hypertrophy': Top Publications. BioMedLib Review; BodyPartOrgan;PyloricHypertrophy:706543358. ISSN: 2331-5717. 2014/3/28
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  • [Title] 'Body PartsCMMA OrgansCMMA or Organ Components' associated with 'Pyloric Hypertrophy': Top Publications.
  • [Transliterated title]
  • Background: There are articles published each month which present 'Body Part Organ or Organ Component' for 'pyloric hypertrophy'.
  • Finding such articles is important for researchers, clinicians, and patients.
  • However these articles are spread across thousands of journals, and there are many types of 'Body Part Organ or Organ Component'.
  • This makes searching and locating the relevant publications a challenge.
  • We have used BioMedLib's semantic search technology to address the issue, and gathered all the pertinent publications in this review article.
  • Methods: We categorized the publications we found into two groups.
  • We used the strength of textual-association to separate the groups.
  • In group one there are publications with the strongest evidence of association. We focused finding the most relevant publications pertinent to our goal, rather than combining them into a conclusion section. Such textual synthesis will be the focus of our next project.
  • Results: Group one includes 23 publications, and group two 863 publications.
  • Here are the top 10.
  • Cooper IF et al: 'Hormones' associated with 'Pyloric Hypertrophy': Top Publications.
  • Dodge JA et al: Induction of pyloric hypertrophy by pentagastrin. An animal model for infantile hypertrophic pyloric stenosis.
  • Tanner MS et al: Functional intestinal obstruction due to deficiency of argyrophil neurones in the myenteric plexus. Familial syndrome presenting with short small bowel, malrotation, and pyloric hypertrophy.
  • Tiao MM et al: Antral web associated with distal antral hypertrophy and prepyloric stenosis mimicking hypertrophic pyloric stenosis.
  • Walter MC et al: Acquired antral pyloric hypertrophy in the dog.
  • Badosa Gallart J: [Pyloric hypertrophy in adults].
  • Nezelof C et al: [Familial syndrome combining short small intestine, intestinal malrotation, pyloric hypertrophy and brain malformation. 3 anatomoclinical case reports].
  • Heidenblut A: [Focal pyloric hypertrophy. Anatomy, physiology, pathophysiology and roentgen diagnosis of the pylorus].
  • Ortíz de Solorzano Aurusa J et al: [Pyloric hypertrophy of the adult. Presentation of 4 cases].
  • Swischuk LE et al: Atypical muscle hypertrophy in pyloric stenosis.

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 706543358.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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16. Inoue Y, Miyashita F, Koga M, Yamada N, Toyoda K, Minematsu K: Panmedullary edema with inferior olivary hypertrophy in bilateral medial medullary infarction. J Stroke Cerebrovasc Dis; 2014 Mar;23(3):554-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Panmedullary edema with inferior olivary hypertrophy in bilateral medial medullary infarction.
  • Inferior olivary nucleus hypertrophy results from a pathologic lesion in the Guillain-Mollaret triangle.
  • The relationship between inferior olivary nucleus hypertrophy and the medullary lesion is obscure.
  • To the best of our knowledge, only 1 autopsy case with unilateral medial medullary infarction that was associated with ipsilateral inferior olivary nucleus hypertrophy has been reported.
  • We describe a rare case with acute infarction in the bilateral medial medulla oblongata accompanied by subacute bilateral inferior olivary nucleus hypertrophy and panmedullary edema.
  • The hypertrophy appeared to have been caused by local ischemic damage to the termination of the central tegmental tract at the bilateral inferior olivary nucleus.
  • [MeSH-major] Brain Edema / diagnosis. Brain Stem Infarctions / diagnosis. Medulla Oblongata / pathology. Olivary Nucleus / pathology
  • [MeSH-minor] Angiography, Digital Subtraction. Cerebral Angiography / methods. Diffusion Magnetic Resonance Imaging. Humans. Hypertrophy. Male. Middle Aged. Predictive Value of Tests

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  • [Copyright] Copyright © 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.
  • (PMID = 23601374.001).
  • [ISSN] 1532-8511
  • [Journal-full-title] Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
  • [ISO-abbreviation] J Stroke Cerebrovasc Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Guillain–Mollaret triangle / intracranial dissection / medullary infarction / olivary nucleus hypertrophy
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17. 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.

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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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18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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19. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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20. Xiao J, Xu T, Li J, Lv D, Chen P, Zhou Q, Xu J: Exercise-induced physiological hypertrophy initiates activation of cardiac progenitor cells. Int J Clin Exp Pathol; 2014;7(2):663-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exercise-induced physiological hypertrophy initiates activation of cardiac progenitor cells.
  • OBJECTIVE: Physiological hypertrophy is featured by the hypertrophy of pre-existing cardiomyocytes and the formation of new cardiomyocytes.
  • C-kit positive cardiac progenitor cells increased their numbers in exercise-induced physiological hypertrophy.
  • METHODS: Physiological hypertrophy was induced by swimming and the mRNA levels of GATA binding protein 4 (GATA4), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endogenous hepatocyte growth factor (HGF), and insulin like growth factor-1 (IGF-1) from the whole heart were determined by real-time polymerase chain reactions (RT-PCRs) analysis.
  • CONCLUSION: This study presents that swimming-induced physiological hypertrophy initiates activation of cardiac progenitor cells.
  • [MeSH-minor] Adaptation, Physiological. Animals. Antigens, Ly / genetics. Antigens, Ly / metabolism. Atrial Natriuretic Factor / genetics. Atrial Natriuretic Factor / metabolism. GATA4 Transcription Factor / genetics. GATA4 Transcription Factor / metabolism. Gene Expression Regulation. Hepatocyte Growth Factor / genetics. Hepatocyte Growth Factor / metabolism. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / metabolism. Male. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mice. Mice, Inbred C57BL. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism. RNA, Messenger / metabolism. Swimming. Time Factors. Ventricular Remodeling

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  • (PMID = 24551287.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Ly; 0 / GATA4 Transcription Factor; 0 / Gata4 protein, mouse; 0 / HGF protein, mouse; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / insulin-like growth factor-1, mouse; 114471-18-0 / Natriuretic Peptide, Brain; 67256-21-7 / Hepatocyte Growth Factor; 67763-96-6 / Insulin-Like Growth Factor I; 85637-73-6 / Atrial Natriuretic Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC3925911
  • [Keywords] NOTNLM ; Exercise / cardiac progenitor cells / hypertrophy / physiological
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21. Lin JJ, Riley JD, Hsu DA, Stafstrom CE, Dabbs K, Becker T, Seidenberg M, Hermann BP: Striatal hypertrophy and its cognitive effects in new-onset benign epilepsy with centrotemporal spikes. Epilepsia; 2012 Apr;53(4):677-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Striatal hypertrophy and its cognitive effects in new-onset benign epilepsy with centrotemporal spikes.
  • Despite its signature electroencephalographic pattern and distinct focal motor seizure semiology, little is known about the underlying brain anatomic alteration and the corresponding cognitive consequences.
  • It is of importance to note that the hypertrophy appears to be cognitively adaptive, as enlargement was associated with improved cognitive performances.
  • The anatomic abnormalities and their cognitive effects are evident in a group of children with new- and recent-onset epilepsy, suggesting that the structural brain anomalies occurred before the diagnosis of epilepsy.
  • [MeSH-minor] Adolescent. Brain Mapping. Child. Executive Function / physiology. Female. Head / pathology. Humans. Hypertrophy / etiology. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Neuropsychological Tests

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  • [Copyright] Wiley Periodicals, Inc. © 2012 International League Against Epilepsy.
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  • (PMID = 22360313.001).
  • [ISSN] 1528-1167
  • [Journal-full-title] Epilepsia
  • [ISO-abbreviation] Epilepsia
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / K23 NS060993; United States / NINDS NIH HHS / NS / K23 NS060993; United States / NINDS NIH HHS / NS / K23 NS060993-04; United States / PHS HHS / / R01 44351; United States / NINDS NIH HHS / NS / R01 NS044351; United States / NINDS NIH HHS / NS / R56 NS044351; United States / NINDS NIH HHS / NS / R56 NS044351-08; United States / NCRR NIH HHS / RR / UL1 RR025011
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS360682; NLM/ PMC3321058
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22. Yin X, Peng C, Ning W, Li C, Ren Z, Zhang J, Gao H, Zhao K: miR-30a downregulation aggravates pressure overload-induced cardiomyocyte hypertrophy. Mol Cell Biochem; 2013 Jul;379(1-2):1-6
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  • [Title] miR-30a downregulation aggravates pressure overload-induced cardiomyocyte hypertrophy.
  • miRNAs play an important role in the pathogenesis of cardiac hypertrophy and dysfunction.
  • However, little is known about how miR-30a regulates cardiomyocyte hypertrophy.
  • We assayed miR-30a expression level by real-time PCR and defined the molecular mechanisms of miR-30a-mediated cardiomyocyte hypertrophy.
  • We found that myocardial expression of miR-30a was decreased in mouse models of hypertrophy and in H9c2 cells treated with phenylephrine.
  • MiR-30a inhibition markedly increased mRNA expression of cardiac hypertrophy markers such as atrial natriuretic factor and brain natriuretic peptide in H9c2, and cell size was increased after miR-30a inhibitor treatment.
  • More important, autophagy inhibition suppressed miR-30a inhibitor-induced cardiomyocyte hypertrophy.
  • Together, our data demonstrated that downregulated miR-30a aggravates pressure overload-induced cardiomyocyte hypertrophy by activating autophagy, thus offering a new target for the therapy of cardiomyocyte hypertrophy.
  • [MeSH-minor] 3' Untranslated Regions. Animals. Atrial Natriuretic Factor / genetics. Atrial Natriuretic Factor / metabolism. Autophagy. Cell Line. Cell Size. Down-Regulation. Gene Expression Regulation. HEK293 Cells. Humans. Male. Mice. Mice, Inbred C57BL. Myocardium / metabolism. Myocardium / pathology. Myocytes, Cardiac / metabolism. Myocytes, Cardiac / pathology. Natriuretic Peptide, Brain / genetics. Natriuretic Peptide, Brain / metabolism. Rats

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  • (PMID = 23660952.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / MicroRNAs; 0 / Mirn30d microRNA, mouse; 114471-18-0 / Natriuretic Peptide, Brain; 85637-73-6 / Atrial Natriuretic Factor
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23. Xie YY, Sun MM, Lou XF, Zhang C, Han F, Zhang BY, Wang P, Lu YM: Overexpression of PEP-19 suppresses angiotensin II-induced cardiomyocyte hypertrophy. J Pharmacol Sci; 2014;125(3):274-82
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  • [Title] Overexpression of PEP-19 suppresses angiotensin II-induced cardiomyocyte hypertrophy.
  • The precise molecular mechanisms leading to disturbance of Ca(2+)/calmodulin-dependent intracellular signalling in cardiac hypertrophy remains unclear.
  • As an endogenous calmodulin regulator protein, the pathophysiology role of PEP-19 during cardiac hypertrophy was investigated in the present study.
  • We here demonstrated that PEP-19 protein levels are significantly elevated in the aortic banding model in vivo and angiotensin II-induced cardiomyocyte hypertrophy in vitro.
  • Consistent with inhibitory actions of PEP-19 on cardiomyocyte hypertrophy, induction of CaMKII and calcineurin activation as well as hypertrophy-related genes including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was significantly inhibited by PEP-19 transfection.
  • Together, our results suggest that PEP-19 attenuates angiotensin II-induced cardiomyocyte hypertrophy via suppressing the disturbance of CaMKII and calcineurin signaling.
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / metabolism. Calcineurin / metabolism. Calcium / metabolism. Calcium Signaling. Calcium-Binding Proteins / metabolism. Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism. Calmodulin / metabolism. Cells, Cultured. Hypertrophy / genetics. Male. Natriuretic Peptide, Brain / metabolism. Rats, Sprague-Dawley. Sarcoplasmic Reticulum / metabolism

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  • (PMID = 25048017.001).
  • [ISSN] 1347-8648
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Calmodulin; 0 / Calmodulin-Binding Proteins; 0 / Nerve Tissue Proteins; 0 / Pcp4 protein, rat; 0 / phospholamban; 11128-99-7 / Angiotensin II; 114471-18-0 / Natriuretic Peptide, Brain; 85637-73-6 / Atrial Natriuretic Factor; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 3.1.3.16 / Calcineurin; SY7Q814VUP / Calcium
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24. Xiao J, Li J, Xu T, Lv D, Shen B, Song Y, Xu J: Pregnancy-induced physiological hypertrophy protects against cardiac ischemia-reperfusion injury. Int J Clin Exp Pathol; 2014;7(1):229-35
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  • [Title] Pregnancy-induced physiological hypertrophy protects against cardiac ischemia-reperfusion injury.
  • OBJECTIVE: Cardiac hypertrophy is a compensatory response of the heart to maintain its pumping capacity.
  • Cardiac hypertrophy can be divided into pathological hypertrophy and physiological hypertrophy.
  • The major forms of physiological hypertrophy include developing in response to developmental maturation, exercise, and pregnancy, which is adaptive and beneficial.
  • However, there are conflicting reports for the cardiac protective effects of pregnancy-induced hypertrophy.
  • In the present study, we investigated the effects of pregnancy-induced physiological hypertrophy in cardiac ischemia-reperfusion injury and if cardiac progenitor cells were activated during pregnancy.
  • METHODS: Physiological hypertrophy was induced in pregnancy and the mRNA levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were determined by real-time polymerase chain reactions (RT-PCRs) analysis.
  • Pregnancy-induced physiological hypertrophy protected against cardiac ischemia-reperfusion injury.
  • CONCLUSION: This study presents that pregnancy-induced physiological hypertrophy activates cardiac progenitor cells and thereafter protects against cardiac ischemia-reperfusion injury.
  • [MeSH-minor] Animals. Atrial Natriuretic Factor / biosynthesis. Blotting, Western. Female. Fluorescent Antibody Technique. Mice. Mice, Inbred C57BL. Natriuretic Peptide, Brain / biosynthesis. Organ Size. RNA, Messenger / analysis. Real-Time Polymerase Chain Reaction

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  • (PMID = 24427343.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 114471-18-0 / Natriuretic Peptide, Brain; 85637-73-6 / Atrial Natriuretic Factor
  • [Other-IDs] NLM/ PMC3885477
  • [Keywords] NOTNLM ; Pregnancy / cardiac progenitor cells / hypertrophy / ischemia/reperfusion / physiological
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25. 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; AB6MNQ6J6L / Succinic Acid; EC 1.9.3.1 / Electron Transport Complex IV; EJ27X76M46 / coenzyme Q10; H4N855PNZ1 / alpha-Tocopherol; JMS50MPO89 / Losartan
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26. 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


27. Lu Y, Akinwumi BC, Shao Z, Anderson HD: Ligand activation of cannabinoid receptors attenuates hypertrophy of neonatal rat cardiomyocytes. J Cardiovasc Pharmacol; 2014 Nov;64(5):420-30
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  • [Title] Ligand activation of cannabinoid receptors attenuates hypertrophy of neonatal rat cardiomyocytes.
  • As cardiac hypertrophy is a convergence point of risk factors for heart failure, we determined a role for endocannabinoids in attenuating endothelin-1-induced hypertrophy and probed the signaling pathways involved.
  • The cannabinoid receptor ligand anandamide and its metabolically stable analog, R-methanandamide, suppressed hypertrophic indicators including cardiomyocyte enlargement and fetal gene activation (ie, the brain natriuretic peptide gene) elicited by endothelin-1 in isolated neonatal rat ventricular myocytes.
  • Accordingly, a CB2-selective agonist, JWH-133, prevented only myocyte enlargement but not brain natriuretic peptide gene activation.
  • A CB1/CB2 dual agonist with limited brain penetration, CB-13, inhibited both hypertrophic indicators.
  • In conclusion, CB-13 inhibits cardiomyocyte hypertrophy through AMPK-eNOS signaling and may represent a novel therapeutic approach to cardioprotection.

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  • (PMID = 24979612.001).
  • [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
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28. Yan S, Wu S, Sun L, Jiang B, Tu Z, Xiao X: [Expression of nucleolin in pressure overload-induced cardiac hypertrophy rats]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2014 Feb;39(2):124-8
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  • [Title] [Expression of nucleolin in pressure overload-induced cardiac hypertrophy rats].
  • OBJECTIVE: To detect the expression of nucleolin in cardiac hypertrophy rats induced by pressure overload.
  • Cardiac hypertrophy model was employed by transverse aortic constriction surgery.
  • Nucleolin in the heart, brain and kidney was respectively detected with Western blot.
  • RESULTS: Compared with the sham surgery group, HMI, LVMI in the TAC group increased significantly (P<0.01) 4 weeks after the surgery; the expression of β-MHC mRNA in the heart tissue increased (P<0.05) in the TAC group 4 weeks after the surgery; and the expression of nucleolin protein in the heart tissue of the TAC group was remarkably upregulated (P<0.05) 2 weeks after the surgery, with no change in the brain and kidney tissue between the 2 groups.
  • CONCLUSION: Expression of nucleolin protein has been upregulated in response to pressure overload, which may suggest that nucleolin plays a role in cardiac hypertrophy induced by pressure overload.

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  • (PMID = 24608397.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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29. 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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30. 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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  • [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

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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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31. 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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32. Le Douce V, Cherrier T, Riclet R, Rohr O, Schwartz C: The many lives of CTIP2: from AIDS to cancer and cardiac hypertrophy. J Cell Physiol; 2014 May;229(5):533-7
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  • [Title] The many lives of CTIP2: from AIDS to cancer and cardiac hypertrophy.
  • Initial works have shown the importance of CTIP2 in the establishment and persistence of HIV latency in microglial cells, the main latent/quiescent viral reservoir in the brain.
  • Recent studies have highlighted the importance of CTIP2 in several other pathologies, such as cardiac hypertrophy and various types of human malignancies.


33. 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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34. 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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  • (PMID = 22892919.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3400165
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35. 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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36. Li MH, Zhang YJ, Yu YH, Yang SH, Iqbal J, Mi QY, Li B, Wang ZM, Mao WX, Xie HG, Chen SL: Berberine improves pressure overload-induced cardiac hypertrophy and dysfunction through enhanced autophagy. Eur J Pharmacol; 2014 Apr 5;728:67-76
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  • [Title] Berberine improves pressure overload-induced cardiac hypertrophy and dysfunction through enhanced autophagy.
  • Cardiac hypertrophy is a maladaptive change in response to pressure overload, and is also an important risk for developing heart failure.
  • Berberine is known to have cardioprotective effects in patients with hypertension and in animal models of cardiac hypertrophy.
  • In the current study, we observed that transverse aortic contraction (TAC) surgery induced a marked increase in heart size, the ratio of heart weight to body weight, cardiomyocyte apoptosis, myocardial fibrosis, and hypertrophic marker brain natriuretic peptide, all of which were effectively suppressed by berberine administration.
  • Furthermore, use of autophagy inhibitor 3-methyladenine (3-MA) blocked berberine-induced autophagy level, and abrogated the protection of berberine against heart hypertrophy, cardiac dysfunction, and apoptosis.
  • We conclude that berberine could attenuate left ventricular remodeling and cardiomyocyte apoptosis through an autophagy-dependent mechanism in a rat model of cardiac hypertrophy, which is, at least in part, associated with enhanced autophagy through inhibition of mTOR, p38 and ERK1/2 MAPK signaling pathways.

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  • [Copyright] Copyright © 2014 Elsevier B.V. All rights reserved.
  • (PMID = 24508518.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Grant] United Kingdom / Department of Health / / 1009; United Kingdom / British Heart Foundation / / PG/13/74/30264
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 0I8Y3P32UF / Berberine; 63231-63-0 / RNA
  • [Keywords] NOTNLM ; Autophagy / Berberine / Berberine chloride (PubChem CID: 12456) / Endoplasmic reticulum stress / Hypertrophy / Transverse aortic constriction
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37. Nam YS, Kim Y, Joung H, Kwon DH, Choe N, Min HK, Kim YS, Kim HS, Kim DK, Cho YK, Kim YH, Nam KI, Choi HC, Park DH, Suk K, Lee IK, Ahn Y, Lee CH, Choi HS, Eom GH, Kook H: Small heterodimer partner blocks cardiac hypertrophy by interfering with GATA6 signaling. Circ Res; 2014 Aug 15;115(5):493-503
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  • [Title] Small heterodimer partner blocks cardiac hypertrophy by interfering with GATA6 signaling.
  • OBJECTIVE: We aimed to investigate the role of SHP in adult heart in association with cardiac hypertrophy.
  • METHODS AND RESULTS: The roles of SHP in cardiac hypertrophy were tested in primary cultured cardiomyocytes and in animal models.
  • Hypertrophic stresses repressed the expression of SHP, whereas forced expression of SHP blocked the development of hypertrophy in cardiomyocytes.
  • Metformin, an antidiabetic agent, induced SHP and suppressed cardiac hypertrophy.

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  • [Copyright] © 2014 American Heart Association, Inc.
  • (PMID = 25015078.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Keywords] NOTNLM ; GATA6 transcription factor / hypertrophy / metformin / nuclear receptor subfamily 0, group B, member 2 / orphan nuclear receptors
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38. 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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39. Kang YM, Suk KS, Lee BH, Kim HS, Lee KI, Park SY, Lee HM, Moon SH: Herniated intervertebral disk induces hypertrophy and ossification of ligamentum flavum. J Spinal Disord Tech; 2014 Oct;27(7):382-9
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  • [Title] Herniated intervertebral disk induces hypertrophy and ossification of ligamentum flavum.
  • OBJECTIVES: To investigate the role and effect of degenerated and herniated IVDs on LF hypertrophy and ossification.
  • SUMMARY OF BACKGROUND DATA: Spinal stenosis is caused, in part, by hypertrophy and ossification of the LF, which are induced by aging and degenerative process.
  • CONCLUSIONS: Degenerated and herniated IVDs provide an important pathomechanism in hypertrophy and ossification of the LF through inflammatory cytokines.
  • [MeSH-minor] Aged. Alkaline Phosphatase / metabolism. Cells, Cultured. Collagen / genetics. Collagen / metabolism. Cytokines / metabolism. Dinoprostone / immunology. Dinoprostone / metabolism. Humans. Hypertrophy / immunology. Hypertrophy / pathology. Immunologic Factors. Interleukin-1alpha / immunology. Interleukin-1alpha / metabolism. Interleukin-6 / immunology. Interleukin-6 / metabolism. Intervertebral Disc / immunology. Intervertebral Disc / pathology. Intervertebral Disc / surgery. Middle Aged. Nitric Oxide / metabolism. Osteocalcin / genetics. Osteocalcin / metabolism. RNA, Messenger / metabolism. Spinal Stenosis / immunology. Spinal Stenosis / pathology. Spinal Stenosis / surgery. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 25250946.001).
  • [ISSN] 1539-2465
  • [Journal-full-title] Journal of spinal disorders & techniques
  • [ISO-abbreviation] J Spinal Disord Tech
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / IL6 protein, human; 0 / Immunologic Factors; 0 / Interleukin-1alpha; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 104982-03-8 / Osteocalcin; 31C4KY9ESH / Nitric Oxide; 9007-34-5 / Collagen; EC 3.1.3.1 / Alkaline Phosphatase; K7Q1JQR04M / Dinoprostone
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40. Aguiar CJ, Rocha-Franco JA, Sousa PA, Santos AK, Ladeira M, Rocha-Resende C, Ladeira LO, Resende RR, Botoni FA, Barrouin Melo M, Lima CX, Carballido JM, Cunha TM, Menezes GB, Guatimosim S, Leite MF: Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation. Cell Commun Signal; 2014;12(1):78
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  • [Title] Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation.
  • RESULTS: We found that succinate causes cardiac hypertrophy in a GPR91 dependent manner.
  • Furthermore, we found that serum levels of succinate are increased in patients with cardiac hypertrophy associated with acute and chronic ischemic diseases.
  • CONCLUSIONS: These results show for the first time that succinate plays an important role in cardiomyocyte hypertrophy through GPR91 activation, and extend our understanding of how ischemia can induce hypertrophic cardiomyopathy.

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  • (PMID = 25539979.001).
  • [ISSN] 1478-811X
  • [Journal-full-title] Cell communication and signaling : CCS
  • [ISO-abbreviation] Cell Commun. Signal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4296677
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41. 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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42. 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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43. Onishi E, Sakamoto A, Murata S, Nakamura S, Matsushita M: Unilateral atlantal lateral mass hypertrophy associated with atlanto-occipital fusion. Eur Spine J; 2013 May;22 Suppl 3:S429-33
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  • [Title] Unilateral atlantal lateral mass hypertrophy associated with atlanto-occipital fusion.
  • PURPOSE: Unilateral hypertrophy of the lateral mass of the atlas is an extremely rare condition.
  • The authors present a rare type of unilateral atlantal mass hypertrophy with atlanto-occipital fusion which is associated with an invaginated lateral mass of the atlas and the odontoid process into the foramen magnum.
  • CONCLUSIONS: To our knowledge, such a case of unilateral atlantal mass hypertrophy associated with atlanto-occipital fusion has not been described previously.
  • The authors discuss the pathology of this case and review the literature on unilateral atlantal mass hypertrophy and associated anomalies of the upper cervical spine.
  • [MeSH-minor] Decompression, Surgical. Female. Functional Laterality. Humans. Hypertrophy. Middle Aged. Spinal Cord Compression / etiology. Spinal Cord Compression / surgery

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  • [ISSN] 1432-0932
  • [Journal-full-title] European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society
  • [ISO-abbreviation] Eur Spine J
  • [Language] eng
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44. 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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45. Anderson WJ, Lipworth BJ, Rekhraj S, Struthers AD, George J: Left ventricular hypertrophy in COPD without hypoxemia: the elephant in the room? Chest; 2013 Jan;143(1):91-7
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  • [Title] Left ventricular hypertrophy in COPD without hypoxemia: the elephant in the room?
  • Left ventricular hypertrophy (LVH) is a pivotal cardiovascular risk factor.
  • [MeSH-major] Hypertrophy, Left Ventricular / complications. Pulmonary Disease, Chronic Obstructive / complications
  • [MeSH-minor] Aged. Case-Control Studies. Echocardiography. Female. Humans. Male. Middle Aged. Natriuretic Peptide, Brain / blood. Oximetry. Pilot Projects. Risk Factors. Sex Factors. Spirometry

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  • (PMID = 22797769.001).
  • [ISSN] 1931-3543
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 114471-18-0 / Natriuretic Peptide, Brain
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46. Bessa JM, Morais M, Marques F, Pinto L, Palha JA, Almeida OF, Sousa N: Stress-induced anhedonia is associated with hypertrophy of medium spiny neurons of the nucleus accumbens. Transl Psychiatry; 2013;3:e266
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  • [Title] Stress-induced anhedonia is associated with hypertrophy of medium spiny neurons of the nucleus accumbens.
  • As the NAc is a key component in the neural circuitry of reward, it has been hypothesized that anhedonia, a core symptom of depression, might be related to dysfunction of this brain region.
  • Data show that animals displaying anhedonic behavior display an hypertrophy of medium spiny neurons in the NAc and, in parallel, have increased expression of the genes encoding for brain-derived neurotrophic factor, neural cell adhesion molecule and synaptic protein synapsin 1.
  • [MeSH-minor] Animals. Antidepressive Agents / pharmacology. Behavior, Animal. Fluoxetine / pharmacology. Hypertrophy. Imipramine / pharmacology. Male. Rats. Rats, Wistar. Real-Time Polymerase Chain Reaction

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  • (PMID = 23736119.001).
  • [ISSN] 2158-3188
  • [Journal-full-title] Translational psychiatry
  • [ISO-abbreviation] Transl Psychiatry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antidepressive Agents; 01K63SUP8D / Fluoxetine; OGG85SX4E4 / Imipramine
  • [Other-IDs] NLM/ PMC3693402
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47. Pujadas L, Gruart A, Bosch C, Delgado L, Teixeira CM, Rossi D, de Lecea L, Martínez A, Delgado-García JM, Soriano E: Reelin regulates postnatal neurogenesis and enhances spine hypertrophy and long-term potentiation. J Neurosci; 2010 Mar 31;30(13):4636-49
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  • [Title] Reelin regulates postnatal neurogenesis and enhances spine hypertrophy and long-term potentiation.
  • Reelin, an extracellular protein essential for neural migration and lamination, is also expressed in the adult brain.
  • In the hippocampus, the overexpression of Reelin resulted in an increase in synaptic contacts and hypertrophy of dendritic spines.
  • Our results indicate that Reelin levels in the adult brain regulate neurogenesis and migration, as well as the structural and functional properties of synapses.
  • These observations suggest that Reelin controls developmental processes that remain active in the adult brain.

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  • (PMID = 20357114.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules, Neuronal; 0 / Extracellular Matrix Proteins; 0 / Nerve Tissue Proteins; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / reelin protein
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48. 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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49. 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; 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; United States / NIAMS NIH HHS / AR / R00 AR054793-03; 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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50. 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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