Title of article :
Exercise-induced cardioprotection against myocardial ischemia–reperfusion injury
Author/Authors :
Scott K. Powers، نويسنده , , John C. Quindry*، نويسنده , , Andreas N. Kavazis، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2008
Abstract :
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.
Keywords :
antioxidants , free radicals , heat shock proteins , heart , Ischemia–reperfusion
Journal title :
Free Radical Biology and Medicine
Journal title :
Free Radical Biology and Medicine