| Literature DB >> 19573532 |
Mahipal Singh1, Cerrone R Foster, Suman Dalal, Krishna Singh.
Abstract
Remodeling after myocardial infarction (MI) associates with left ventricular (LV) dilation, decreased cardiac function and increased mortality. The dynamic synthesis and breakdown of extracellular matrix (ECM) proteins play a significant role in myocardial remodeling post-MI. Expression of osteopontin (OPN) increases in the heart post-MI. Evidence has been provided that lack of OPN induces LV dilation which associates with decreased collagen synthesis and deposition. Inhibition of matrix metalloproteinases, key players in ECM remodeling process post-MI, increased ECM deposition (fibrosis) and improved LV function in mice lacking OPN after MI. This review summarizes--1) signaling pathways leading to increased expression of OPN in the heart; 2) the alterations in the structure and function of the heart post-MI in mice lacking OPN; and 3) mechanisms involved in OPN-mediated ECM remodeling post-MI. Published by Elsevier Ltd.Entities:
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Year: 2009 PMID: 19573532 PMCID: PMC2823840 DOI: 10.1016/j.yjmcc.2009.06.015
Source DB: PubMed Journal: J Mol Cell Cardiol ISSN: 0022-2828 Impact factor: 5.000