title: Ischemia-reperfusion-induced cardiac injury: a brief review.
abstract: 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.
authors.affiliation: Department of Applied Physiology and Kinesiology, Center for Exercise Science, University of Florida, Gainesville, FL 32611, USA. spowers@hhp.ufl.edu
authors.forename: Scott K
authors.initials: SK
authors.lastname: Powers
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Murlasits
authors.forename: Min
authors.initials: M
authors.lastname: Wu
authors.forename: Andreas N
authors.initials: AN
authors.lastname: Kavazis
mesh_terms: D017209:Apoptosis; D006801:Humans; D000860:Hypoxia; D019157:Ischemic Preconditioning, Myocardial; D009336:Necrosis; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control