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.
Singh, Mahipal; Foster, Cerrone R.; Dalal, Suman; and Singh, Krishna. 2010. Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI. Journal of Molecular and Cellular Cardiology. Vol.48(3). 538-543. https://doi.org/10.1016/j.yjmcc.2009.06.015 ISSN: 0022-2828