细胞凋亡的线粒体途径与缺血缺氧性肾损伤

Mitochondrial death pathway and renal ischemia-reperfusion injury

"外源性通路"和"内源性通路"是细胞内凋亡信号转导的两条基本途径。线粒体作为内源性通路的中心环节在其中起主导作用。细胞凋亡时线粒体膜通透性增加,释放可溶性膜间隙蛋白(细胞色素,凋亡诱导因子,Smac/DIABLO等),启动caspase级联反应和不依赖caspase途径的方式参与凋亡发生。Bcl-2蛋白家族以线粒体为靶位调控凋亡。线粒体凋亡途径也参与了肾缺血再灌注的损伤,其中炎症反应与细胞凋亡发生交互作用使得其损伤机制更为复杂。

Two major pathways for induction of apoptosis have been identified intrinsic and extrinsic. The intrinsic pathway for apoptosis involves the participation of mitochondria, which releases caspase-activating proteins, such as cytochrome C and so on. Apoptosis induced factor within mitochondria is believed to be directly in the induction of apoptosis. Bcl-2 protein family regulate apoptosis through mitochondria. The intrinsic pathway is also involved in renal ischemia-reperfusion injury, but the mechanisms are more complicated on account of the crosstalk between inflammation and apoptosis. In this review, we summarized recent advances in the understanding of the intrinsic pathway and the relationship between the mitochondria pathway and renal ischemia-reperfusion injury.