摘要
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.
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, isehemic postconditioning and pharmaeological 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 myoeardium and limiting infarct size during myocardial ischemia - reperfusion.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2009年第10期2062-2067,共6页
Chinese Journal of Pathophysiology
基金
福建医科大学附属协和医院重点学科基金资助项目(No.协院科2005113)
关键词
PI3K-AKT
ERK1/2
预处理
后处理
心肌再灌注损伤
Phosphatidylinositol -3 -OH kinase -Akt
p42/p44 extracellular signal -regulated protein kinases
Preconditioning
Postconditioning
Myocardial reperfusion injury
