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Cardioprotection against reperfusion injury: updated mechanisms and strategies

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Author:: No author available

Journal Title:: ACTA PHYSIOLOGICA SINICA

Issue:: 5

DOI:: 10.3321/j.issn:0371-0874.2007.05.003

Key Word:: 再灌注损伤;心脏保护;G蛋白耦联受体;胰岛素;缺血后处理;线粒体膜通透性转换孔;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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