RISK信号通路在心肌预处理及后处理中的作用  

RISK signaling pathway in myocardial preconditioning and postconditioning

作　　者：方军[1,2] 吴黎明[1,3] 陈良龙[1,2] 

机构地区：[1]福建医科大学附属协和医院心内科 [2]福建省冠心病研究所 [3]福建省老年医学研究所,福建福州350001

出　　处：《中国病理生理杂志》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)

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.

关 键 词：PI3K-AKT ERK1/2 预处理 后处理 心肌再灌注损伤 

分 类 号：R541.4[医药卫生—心血管疾病] R363[医药卫生—内科学]