Mitochondrial redox signaling during apoptosis
Mitochondrial redox signaling during apoptosis
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DOI：
10.1023/a:1005423818280
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发表时间：
1999-08-01
影响因子：
3
通讯作者：
Jones, DP
中科院分区：
文献类型：
--
作者：
Cai, JY;Jones, DP
细胞氧化还原状态在细胞凋亡中的调节作用仍有争议。早期的氧化还原信号可以将上游的不同信号传递到线粒体并启动细胞凋亡。另一方面，线粒体细胞色素c的释放触发活性氧（ROS）的产生，并使凋亡细胞更加氧化。虽然连续的半胱天冬酶激活不具有明显的氧化还原敏感性组分，但氧化还原信号传导提供了与半胱天冬酶级联反应平行的单独途径。凋亡相关的氧化还原变化的功能尚不清楚，它可能提供正反馈机制，如激活线粒体通透性转换和凋亡信号激酶（ASK-1）。由于凋亡细胞被指定为被快速消除，因此急剧的细胞氧化可能参与凋亡小体的最终降解，甚至参与吞噬后蛋白水解活性的终止。
The regulatory role of cellular redox state during apoptosis is still controversial. Early redox signaling can transduce divergent upstream signals to mitochondria and initiate apoptosis. On the other hand, release of mitochondrial cytochrome c triggers generation of reactive oxygen species (ROS) and renders apoptotic cells much more oxidized. Although the sequential caspase activation does not have apparent redox-sensitive components, redox signaling provides a separate pathway that is parallel with the caspase cascade. The function of the apoptosis-associated redox change is uncertain, it could provide positive feedback mechanisms, such as activating mitochondrial permeability transition and apoptosis signaling kinase (ASK-1). Since apoptotic cells are designated to be quickly eliminated, the dramatic cellular oxidation could be involved in the final degradation of apoptotic bodies and even the termination of the proteolytic activity after phagocytosis.