Journal
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
Volume 39, Issue 9, Pages 1529-1536Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/mss.0b013e3180d099c1
Keywords
heart; anoxia; necrosis; apoptosis; cardioprotection
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Funding
- NHLBI NIH HHS [R01 HL067855] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL067855] Funding Source: NIH RePORTER
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Myocardial ischemia-reperfusion (IR) injury is the primary contributor to the morbidity and mortality associated with coronary artery disease. Depending on the duration of ischemia, three levels of IR-induced cardiac injury have been identified. The cellular events leading to IR-induced cellular injury are complex, but the key elements include IR-induced radical production, cellular disturbances in calcium homeostasis, and activation of cellular proteases. Moreover, growing evidence indicates that mitochondrial injury plays a major role in IR-induced injury, because mitochondria seem to be the final arbitrators of IR-induced cell death and determine whether the myocyte will die from necrosis or apoptosis. This review will provide a brief summary of our current understanding of the cellular events that contribute to IR-induced cardiac injury and cell death. Further, we will briefly introduce the concept of cardioprotection and outline several successful approaches that can induce a cardioprotective phenotype. Finally, in hopes of stimulating future research, this review will also identify important gaps in our knowledge of IR-induced myocardial injury.
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