The protective roles of autophagy in ischemic preconditioning  

作　　者：Wen-jun YAN Hai-long DONG Li-ze XIONG 

机构地区：[1]Department of Anesthesiology, Gansu Provincial Hospital, Lanzhou 730000, China [2]Department of Anesthesiology, Xijing Hospital,Fourth Military Medical University, Xi-an 710032, China

出　　处：《Acta Pharmacologica Sinica》2013年第5期636-643,共8页中国药理学报（英文版）

基　　金：Acknowledgements This work was supported by the National Science Foundation for Distinguished Young Scholars （Grant 30725039） and the key project for the National Natural Science Foundation of China （Grant 30930091）.

摘　　要：a process for the degradation of protein aggregates and dysfunctional organelles, is required for cellular homeostasis and cell survival in response to stress and is implicated in endogenous protection. Ischemic preconditioning is a brief and nonlethal episode of ischemia, confers protection against subsequent ischemia-reperfusion through the up-regulation of endogenous protec- tive mechanisms. Emerging evidence shows that autophagy is associated with the protective effect of ischemic preconditioning. This review summarizes recent progress in research on the functions and regulations of the autophagy pathway in preconditioning-induced protection and cellular survival.a process for the degradation of protein aggregates and dysfunctional organelles, is required for cellular homeostasis and cell survival in response to stress and is implicated in endogenous protection. Ischemic preconditioning is a brief and nonlethal episode of ischemia, confers protection against subsequent ischemia-reperfusion through the up-regulation of endogenous protec- tive mechanisms. Emerging evidence shows that autophagy is associated with the protective effect of ischemic preconditioning. This review summarizes recent progress in research on the functions and regulations of the autophagy pathway in preconditioning-induced protection and cellular survival.

关 键 词：AUTOPHAGY ischemia-reperfusion injury ischemic preconditioning AMPK MTOR BECLINL P13K MITOCHONDRIA endoplasmicreticulum stress reactive oxygen species （ROS） apoptosis 

分 类 号：Q463[生物学—生理学] Q523