Document Detail


Three 4-letter words of hypertension-related cardiac hypertrophy: TRPC, mTOR, and HDAC.
MedLine Citation:
PMID:  21320507     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Left ventricular hypertrophy due to hypertension represents a major risk factor for adverse cardiovascular events and death. In recent years, the prevalence of cardiac hypertrophy has increased due to obesity and an aging population. Notably, a significant number of individuals have persistent cardiac hypertrophy in the face of blood pressure that is normalized by drug treatment. Thus, a better understanding of the processes underlying the cardiac remodeling events that are set into play by hypertension is needed. At the level of the cardiac myocytes, hypertrophic growth is often described as physiological, as occurs with exercise, or pathological, as seen with hypertension. Here we discuss recent developments in three areas that are fundamental to pathological hypertrophic growth of cardiac myocytes. These areas are the transient receptor potential canonical (TRPC) channels, mammalian target of rapamycin (mTOR) complexes, and histone deacetylase (HDAC) enzymes. In the last several years, studies in each of these areas have yielded new and exciting discoveries into the genesis of pathological growth of cardiac myocytes. The phosphoinositide 3-kinase-Akt signaling network may be the common denominator that links these areas together. Defining the interrelationship among TRPC channels, mTOR signaling, and HDAC enzymes is a promising, but challenging area of research. Such knowledge will undoubtedly lead to new drugs that better prevent or reverse left ventricular hypertension.
Authors:
Mazen Kurdi; George W Booz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-02-19
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  50     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-10     Completed Date:  2011-09-26     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  964-71     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Chemistry and Biochemistry, Faculty of Sciences, Lebanese University, Rafic Hariri Educational Campus, Hadath, Lebanon.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomegaly / etiology*,  physiopathology*
Histone Deacetylases / metabolism*
Humans
Hypertension / complications*,  physiopathology*
Signal Transduction
TOR Serine-Threonine Kinases / metabolism*
TRPC Cation Channels / metabolism*
Grant Support
ID/Acronym/Agency:
R01 HL088101-02S1/HL/NHLBI NIH HHS; R01 HL088101-04/HL/NHLBI NIH HHS; R01HL088101-02S1/HL/NHLBI NIH HHS; R01HL088101-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/TRPC Cation Channels; EC 2.7.1.1/TOR Serine-Threonine Kinases; EC 3.5.1.98/Histone Deacetylases
Comments/Corrections

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