The anti-apoptotic pro-survival kinase signaling cascades,phosphatidylinositol-3-OH kinase(PI3K)-Akt and p42/p44 extra-cellular signal-regulated protein kinases(ERK 1/2),which have been termed the reperfusion injury s...The anti-apoptotic pro-survival kinase signaling cascades,phosphatidylinositol-3-OH kinase(PI3K)-Akt and p42/p44 extra-cellular signal-regulated protein kinases(ERK 1/2),which have been termed the reperfusion injury salvage kinase(RISK)pathway,are involved in cellular survival.In myocardial ischemic preconditioning,pharmacological preconditioning,ischemic postconditioning and pharmacological postconditioning,the activation of these kinase cascades at the time of reperfusion has been demonstrated to confer cardioprotection against reperfusion-induced injury.Targeting the RISK signaling pathway may provide a novel strategy to salvaging viable myocardium and limiting infarct size during myocardial ischemia-reperfusion.展开更多
文摘The anti-apoptotic pro-survival kinase signaling cascades,phosphatidylinositol-3-OH kinase(PI3K)-Akt and p42/p44 extra-cellular signal-regulated protein kinases(ERK 1/2),which have been termed the reperfusion injury salvage kinase(RISK)pathway,are involved in cellular survival.In myocardial ischemic preconditioning,pharmacological preconditioning,ischemic postconditioning and pharmacological postconditioning,the activation of these kinase cascades at the time of reperfusion has been demonstrated to confer cardioprotection against reperfusion-induced injury.Targeting the RISK signaling pathway may provide a novel strategy to salvaging viable myocardium and limiting infarct size during myocardial ischemia-reperfusion.
