Document Detail


Myocardial remodeling in viral heart disease: possible interactions between inflammatory mediators and MMP-TIMP system.
MedLine Citation:
PMID:  14739765     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Matrix metalloproteinases (MMP), a family of proteases, are involved in the degradation of extracellular matrix proteins and hence in the determination of interstitial architecture. In the heart, MMPs have been found to play a significant role in the development of myocardial remodeling and congestive heart failure. Tissue inhibitors of matrix metalloproteinases (TIMPs) represent a family of proteins which are known to regulate the expression and activity of MMPs. TIMPs are endogenous physiological inhibitors of MMPs and their concomitant downregulation in heart failure suggests the existence of a critical balance between MMPs and TIMPs in the normal maintenance of myocardial interstitial homeostasis. In addition, cytokines regulate expression of both MMPs and TIMPs besides eliciting a direct effect on myocardial cell function. Therefore, myocardial inflammation may also contribute to the development of cardiac remodeling along with other stimuli like mechanical stress and humoral factors. Viral myocarditis, a predisposing factor for dilated cardiomyopathy, is a condition in which extent of intramyocardial inflammation is thought to determine the progression of disease. Inflammatory events in the heart following viral infection are speculated to be responsible for the transition of myocarditis to dilated cardiomyopathy. In viral myocarditis and other inflammatory heart diseases, the inflammatory cells and their battery of cytokines may also alter the myocardial MMP-TIMP system and eventually lead to dilation of the heart and ventricular dysfunction. The objective of this review is to present an overall picture of the inflammatory phase in viral myocarditis and discuss the possible interactions between inflammation and myocardial MMP profiles which may lead to the evolution of dilated cardiomyopathy.
Authors:
Matthias Pauschinger; Kumaran Chandrasekharan; Heinz-Peter Schultheiss
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Heart failure reviews     Volume:  9     ISSN:  1382-4147     ISO Abbreviation:  Heart Fail Rev     Publication Date:  2004 Jan 
Date Detail:
Created Date:  2004-01-23     Completed Date:  2004-05-17     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9612481     Medline TA:  Heart Fail Rev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  21-31     Citation Subset:  IM    
Affiliation:
Department of Cardiology, University Hospital Benjamin Franklin, Free University Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany. pauschinger@ukbf.fu-berlin.de
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MeSH Terms
Descriptor/Qualifier:
Cardiomyopathy, Dilated / etiology,  metabolism*
Extracellular Matrix / metabolism*
Humans
Matrix Metalloproteinases / antagonists & inhibitors,  metabolism*
Myocarditis / complications,  physiopathology*,  virology
Tissue Inhibitor of Metalloproteinases / metabolism*
Ventricular Remodeling*
Chemical
Reg. No./Substance:
0/Tissue Inhibitor of Metalloproteinases; EC 3.4.24.-/Matrix Metalloproteinases

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


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