Matrix Metalloproteinases in Myocardial Infarction and Heart Failure

被引:184
作者
DeLeon-Pennell, Kristine Y. [1 ,2 ]
Meschiari, Cesar A. [1 ]
Jung, Mira [1 ]
Lindsey, Merry L. [1 ,2 ]
机构
[1] UMMC, Mississippi Ctr Heart Res, Jackson, MS 39216 USA
[2] GV Sonny Montgomery Vet Affairs Med Ctr, Res Serv, Jackson, MS 39216 USA
来源
MATRIX METALLOPROTEINSES AND TISSUE REMODELING IN HEALTH AND DISEASE: CARDIOVASCULAR REMODELING | 2017年 / 147卷
关键词
DELAYING INFLAMMATION RESOLUTION; LEFT-VENTRICULAR DYSFUNCTION; MACROPHAGE ELASTASE MMP-12; PREVENTS CARDIAC RUPTURE; POSTMYOCARDIAL INFARCTION; EXTRACELLULAR-MATRIX; GENE-EXPRESSION; TISSUE INHIBITOR; CARDIOVASCULAR-DISEASE; ENDOTHELIAL-CELLS;
D O I
10.1016/bs.pmbts.2017.02.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cardiovascular disease is the leading cause of death, accounting for 600,000 deaths each year in the United States. In addition, heart failure accounts for 37% of health care spending. Matrix metalloproteinases (MMPs) increase after myocardial infarction (MI) and correlate with left ventricular dysfunction in heart failure patients. MMPs regulate the remodeling process by facilitating extracellular matrix turnover and inflammatory signaling. Due to the critical role MMPs play during cardiac remodeling, there is a need to better understand the pathophysiological mechanism of MMPs, including the biological function of the downstream products of MMP proteolysis. Future studies developing new therapeutic targets that inhibit specific MMP actions to limit the development of heart failure post-MI are warranted. This chapter focuses on the role of MMPs post-MI, the efficiency of MMPs as biomarkers for MI or heart failure, and the future of MMPs and their cleavage products as targets for prevention of post-MI heart failure.
引用
收藏
页码:75 / 100
页数:26
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