Exercise-induced cardioprotection against myocardial ischemia-reperfusion injury

被引:180
作者
Powers, Scott K. [1 ]
Quindry, John C. [1 ]
Kavazis, Andreas N. [1 ]
机构
[1] Univ Florida, Dept Appl Physiol & Kinesiol, Gainesville, FL 32611 USA
关键词
heart; ischemia-reperfusion; antioxidants; heat shock proteins; free radicals;
D O I
10.1016/j.freeradbiomed.2007.02.006
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
Myocardial ischemia-reperfusion (IR) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. Muscular exercise is a countermeasure to protect against IR-induced cardiac injury in both young and old animals. Specifically, regular bouts of endurance exercise protect the heart against all levels of IR-induced injury. Proposed mechanisms to explain the cardioprotective effects of exercise include alterations in coronary circulation, expression of endoplasmic reticulum stress proteins, increased cyclooxygenase-2 activity, induction of myocardial heat shock proteins, improved cardiac antioxidant capacity, and/or elevation of ATP-sensitive potassium channels on both the sarcolemmal and the mitochondrial inner membranes. Moreover, it seems possible that other, yet to be defined, mechanisms of exercise-induced cardioprotection may also exist. Of the known putative cardioprotective mechanisms, current evidence suggests that elevated myocardial levels of antioxidants and increased expression of sarcolemmal ATP-sensitive potassium channels are both contributors to exercise-induced cardioprotection against IR injury. At present, it is unclear if these two protective mediators act independently or interact to contribute to exercise-induced cardioprotection. Understanding the molecular basis for exercise-induced cardioprotection will provide the required knowledge base to develop therapeutic approaches to protect the heart during an IR insult. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:193 / 201
页数:9
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