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Osteopontin: role in extracellular matrix deposition and myocardial remodeling post-MI Singh M; Foster CR; Dalal S; Singh KJ Mol Cell Cardiol 2010[Mar]; 48 (3): 538-43Remodeling 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.|Animals[MESH]|Extracellular Matrix/*metabolism[MESH]|Humans[MESH]|Mice[MESH]|Models, Biological[MESH]|Myocardial Infarction/*metabolism/physiopathology[MESH]|Myocardium/*metabolism/pathology[MESH]|Osteopontin/metabolism/*physiology[MESH] |
