脑缺氧损伤后线粒体途径神经元凋亡

Mitochondrial apoptotic signaling pathway in neurons following brain injury induced by hypoxia

脑缺氧后神经元线粒体损伤不单使细胞发生能量缺失和功能丧失,还可以介导凋亡调节信号,是缺氧损伤后神经元凋亡的一个中心环节。线粒体膜通透性转变,释放细胞色素C活化特定的caspase蛋白酶,使细胞进入不可逆的凋亡程序中;Bcl-2家族促凋亡和抑制凋亡成员之间相互作用,调控细胞色素C释放,调节线粒体介导的凋亡过程。

Impairment of neuronal mitochondria following hypoxia of brain not only result in nerve cell's energy-deprivation and dysfunction,mitochondria also play key roles in apoptosis of neurons.A central step being the release of cytochrome c(cyt c)across the outer mitochondrial membrane into the cytoplasm through opening of the mitochondrial permeability transition pore.Releasing of cytochrome c induce to downstream consequences of specific caspase activation.The antiapoptotic and proapoptotic members of the Bcl-2family regulate mitochondrial activities relevant to apoptotic signaling by influencing the realaseing of cyt c.