Osteopontin: role in extracellular matrix deposition and myocardial remodeling post-MI.

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.

• Authors: Mahipal Singh, Cerrone R Foster, Suman Dalal, Krishna Singh
• Journal: Journal of molecular and cellular cardiology (J Mol Cell Cardiol) Vol. 48 Issue 3 Pg. 538-43 (Mar 2010) ISSN: 1095-8584 [Electronic] England
• PMID: 19573532 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S., Review)
• Copyright: Published by Elsevier Ltd.

Chemical References

• Osteopontin

Topics

• Animals
• Extracellular Matrix (metabolism)
• Humans
• Mice
• Models, Biological
• Myocardial Infarction (metabolism, physiopathology)
• Myocardium (metabolism, pathology)
• Osteopontin (metabolism, physiology)