心磷脂
线粒体
细胞生物学
细胞色素c
凋亡体
膜间隙
程序性细胞死亡
线粒体膜间隙
氧化应激
活性氧
生物
细胞凋亡
辅酶Q-细胞色素c还原酶
生物化学
半胱氨酸蛋白酶
细菌外膜
磷脂
膜
基因
大肠杆菌
作者
Martin Ott,Vladimir Gogvadze,Sten Orrenius,Boris Zhivotovsky
出处
期刊:Apoptosis
[Springer Nature]
日期:2007-02-09
卷期号:12 (5): 913-922
被引量:1681
标识
DOI:10.1007/s10495-007-0756-2
摘要
In addition to the well-established role of the mitochondria in energy metabolism, regulation of cell death has recently emerged as a second major function of these organelles. This, in turn, seems to be intimately linked to their role as the major intracellular source of reactive oxygen species (ROS), which are mainly generated at Complex I and III of the respiratory chain. Excessive ROS production can lead to oxidation of macromolecules and has been implicated in mtDNA mutations, ageing, and cell death. Mitochondria-generated ROS play an important role in the release of cytochrome c and other pro-apoptotic proteins, which can trigger caspase activation and apoptosis. Cytochrome c release occurs by a two-step process that is initiated by the dissociation of the hemoprotein from its binding to cardiolipin, which anchors it to the inner mitochondrial membrane. Oxidation of cardiolipin reduces cytochrome c binding and results in an increased level of "free" cytochrome c in the intermembrane space. Conversely, mitochondrial antioxidant enzymes protect from apoptosis. Hence, there is accumulating evidence supporting a direct link between mitochondria, oxidative stress and cell death.
科研通智能强力驱动
Strongly Powered by AbleSci AI