Cardioprotection against reperfusion injury: updated mechanisms and strategies

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XI Jin-Kun()
JIN Yuan-Zhe()
CUI Xun()
XU Zhe-Long(XU Zhe-Long,Corresponding author. Tel: +1-919-8434174; Fax: +1-919-8433805; Email:
Journal Title:
Volume 59, Issue 05, 2007
Key Word:
reperfusion injury; cardioprotection; G protein-coupled receptor; insulin; ischemic postconditioning; mitochondrial permeability transition pore

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 3β (GSK-3β), 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.

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