期刊
ANNALS OF MEDICINE
卷 35, 期 5, 页码 316-326出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/07853890310001285
关键词
extracellular matrix; matrix metalloproteinases; MMP inhibitor; myocardial infarction
资金
- NHLBI NIH HHS [R01 HL58081-01, P50-HLO6H, HL-42550, R01 HL61543-01, HL-45024, HL-97012, HL-10337, HL-42250-10/10] Funding Source: Medline
- PHS HHS [P01-48788] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [F32HL010337, R01HL042250, R03HL097012, R01HL058081, R29HL045024, P01HL042550, R01HL061543] Funding Source: NIH RePORTER
While current therapeutic strategies restore blood flow to the ischemic myocardium and limit infarct size, adverse left ventricular (LV) remodeling that progresses to dysfunction remains a significant complication following myocardial infarction (MI). The extracellular matrix (ECM) is a key component in the remodeling process, and increases in collagen occur in the infarct area to replace necrotic myocytes and form a sear. The ECM is coupled to the cell through cell surface receptors, primary of which are the integrins. In addition, the matrix metal loproteinases coordinate ECM turnover through degradation of ECM components. Several laboratories have demonstrated matrix metal loproteinase (MMP) participation in remodeling events that lead to LV dilation, and inhibition or targeted deletion of specific MMPs has beneficial effects post-MI. MMP inhibition is a particular focus of recent studies designed to understand the underlying mechanisms of LV remodeling and to evaluate pharmacologic strategies that target the ECM to affect adverse LV remodeling following MI.
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