Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 48, Issue 3, Pages 538-543Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.yjmcc.2009.06.015
Keywords
Osteopontin; ECM; MMPs; Myocardial infarction; Myocardial remodeling
Categories
Funding
- National Institutes of Health [HL-091405, HL-092459]
- Department of Veterans Affairs
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R21HL091405, R21HL092459] Funding Source: NIH RePORTER
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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.
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