Document Detail


NADPH oxidases and cardiac remodelling.
MedLine Citation:
PMID:  20658317     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A heart under chronic stress undergoes cardiac remodelling, a process that comprises structural and functional changes including cardiomyocyte hypertrophy, interstitial fibrosis, contractile dysfunction, cell death and ventricular dilatation. Reactive oxygen species (ROS)-dependent modulation of intracellular signalling is implicated in the development of cardiac remodelling. Among the different ROS sources that are present in the heart, NADPH oxidases (NOXs) are particularly important in redox signalling. NOX isoforms are expressed in multiple cell types including cardiomyocytes, fibroblasts, endothelial cells and inflammatory cells-with the two main isoforms expressed in the heart being NOX2 and NOX4. Recent studies indicate that NOX-dependent signalling is involved in the development of cardiomyocyte hypertrophy, interstitial fibrosis and post-MI remodelling. NOXs may also be involved in the genesis of contractile dysfunction and myocyte apoptosis. Here, we review the main effects of NOXs in the pathogenesis of cardiac remodelling and the redox-sensitive signalling pathways that underlie these effects. The elucidation of mechanisms involved in NOX-dependent regulation of cardiac remodelling may lead to new therapeutic targets for heart failure.
Authors:
Adam Nabeebaccus; Min Zhang; Ajay M Shah
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Heart failure reviews     Volume:  16     ISSN:  1573-7322     ISO Abbreviation:  Heart Fail Rev     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-20     Completed Date:  2011-04-05     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  9612481     Medline TA:  Heart Fail Rev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5-12     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Apoptosis
Cardiac Catheterization
Endothelium, Vascular
Fibroblasts / metabolism
Humans
Inflammation / pathology
Myocytes, Cardiac / metabolism
NADPH Oxidase / metabolism*
Oxidative Stress*
Reactive Oxygen Species / metabolism*
Signal Transduction
Time Factors
Ventricular Remodeling*
Grant Support
ID/Acronym/Agency:
RG/08/011/25922//British Heart Foundation; //British Heart Foundation
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; EC 1.6.3.1/NADPH Oxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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