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Cardioprotection against reperfusion injury: updated mechanisms and strategies

Xi Jinkun, Jin Yuanzhe, Cui Xun, Xu Zhelong

Department of Anesthesiology, the University of North Carolina at Chapel Hill, Chapel Hill, NC27599；China

Abstract

Early restoration of blood flow to the ischemic myocardium not only saves myocardium but also induces reperfusion injury.While no specific therapy to reduce reperfusion injury has yet been established, recent laboratory studies have shown that G proteincoupled receptor (GPCR) agonists, insulin, and postconditioning can effectively prevent reperfusion injury in various experimental settings and animal species. The potential mechanisms underlying the cardioprotection initiated by these interventions may include activation of the reperfusion injury salvage kinase (RISK) pathway, inactivation of glycogen synthase kinase 3#beta# (GSK-3#beta#), and modulation of mitochondrial permeability transition pore (mPTP) opening. These encouraging laboratory findings may help us develop successful clinical strategies to salvage reperfused myocardium in patients with acute myocardial infarction.

Key words: Reperfusion injury;cardioprotection;G protein-coupled receptor;Insulin;ischemic postconditioning;mitochondrial permeability transition pore

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Citing This Article：

Xi Jinkun, Jin Yuanzhe, Cui Xun, Xu Zhelong. Cardioprotection against reperfusion injury: updated mechanisms and strategies. Acta Physiol Sin 2007; 59 (5): 553-561 (in Chinese with English abstract).