Powers Scott K, Quindry John C, Kavazis Andreas N
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA.
Free Radic Biol Med. 2008 Jan 15;44(2):193-201. doi: 10.1016/j.freeradbiomed.2007.02.006. Epub 2007 Feb 21.
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.
心肌缺血再灌注(IR)损伤是导致冠状动脉疾病相关发病和死亡的主要因素。体育锻炼是一种可防止年轻和老年动物发生IR诱导心脏损伤的对策。具体而言,定期进行耐力运动可保护心脏免受各种程度的IR诱导损伤。用于解释运动心脏保护作用的机制包括冠状动脉循环的改变、内质网应激蛋白的表达、环氧化酶-2活性增加、心肌热休克蛋白的诱导、心脏抗氧化能力的改善和/或肌膜及线粒体内膜上ATP敏感性钾通道的升高。此外,运动诱导心脏保护的其他尚未明确的机制似乎也可能存在。在已知的假定心脏保护机制中,目前的证据表明,心肌抗氧化剂水平升高和肌膜ATP敏感性钾通道表达增加均有助于运动诱导的针对IR损伤的心脏保护。目前尚不清楚这两种保护介质是独立起作用还是相互作用以促成运动诱导的心脏保护。了解运动诱导心脏保护的分子基础将为开发在IR损伤期间保护心脏的治疗方法提供所需的知识库。