Activation of MMP-2 as a key event in oxidative stress injury to the heart

被引:48
作者
Ali, Mohammad A. M. [1 ]
Schulz, Richard [1 ,2 ]
机构
[1] Univ Alberta, Dept Pharmacol, Cardiovasc Res Grp, Edmonton, AB T6G 2S2, Canada
[2] Univ Alberta, Dept Pediat, Cardiovasc Res Grp, Edmonton, AB T6G 2S2, Canada
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷
关键词
Oxidative damage; Reactive oxygen species; Nitric oxide; Peroxynitrite; Matrix metalloproteinases; Ischemia/reperfusion; Sarcomere; Troponin I; Myosin light chain-1; Cardiac dysfunction; ISCHEMIA-REPERFUSION INJURY; MATRIX METALLOPROTEINASE-2 EXPRESSION; ACUTE MYOCARDIAL-ISCHEMIA; PROTEIN S-NITROSYLATION; NITRIC-OXIDE; TISSUE INHIBITOR; SMOOTH-MUSCLE; CARDIOVASCULAR-DISEASE; ATHEROSCLEROTIC PLAQUE; CELLULAR MECHANISMS;
D O I
10.2741/3274
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
Oxygen and nitrogen derived free radicals play a crucial role in both cardiac physiology and pathology. In this review we discuss how these molecules interact in the cardiac cell, some aspects of their physiological importance, and their pathological effects with a special focus on the activation of matrix metalloproteinases (MMPs) as an early event in oxidative stress damage. MMPs are a family of zinc-dependent endopeptidases which play an active role in regulating the extracellular matrix. Recently, however, it has been recognized that MMPs may also rapidly act on intracellular substrates on a minutes timescale. This review will consider some recent developments in the intracellular localization and novel substrates of MMP-2 within the heart. In addition, we will discuss MMP inhibition as a novel therapeutic strategy to prevent oxidative stress damage to the heart.
引用
收藏
页码:699 / 716
页数:18
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