Redox Regulation of Apoptosis before and after Cytochrome C Release.
Redox Regulation of Apoptosis before and after Cytochrome C Release.
复制标题
细胞色素 C 释放前后细胞凋亡的氧化还原调节。
DOI:
10.1080/12265071.2003.9647675
复制
发表时间:
2003
期刊:
影响因子:
--
通讯作者:
Almasan,Alex
中科院分区:
文献类型:
--
作者:
Chen,Quan;Crosby,Meredith;Almasan,Alex
Programmed cell death, or apoptosis, is one of the most studied areas of modern biology. Apoptosis is a genetically regulated process, which plays an essential role in the development and homeostasis of higher organisms. Mitochondria, known to play a central role in regulating cellular metabolism, was found to be critical for regulating apoptosis induced under both physiological and pathological conditions. Mitochondria are a major source of reactive oxygen species (ROS) but they can also serve as its target during the apoptosis process. Release of apoptogenic factors from mitochondria, the best known of which is cytochrome c, leads to assembly of a large apoptosis‐inducing complex called the apoptosome. Cysteine proteases (called caspases) are recruited to this complex and, following their activation by protectlytic cleavage, activate other caspases, which in turn target for specific cleavage a large number of cellular proteins. The redox regulation of apoptosis during and after cytochrome c release is an area of intense investigation. This review summarizes what is known about the biological role of ROS and its targets in apoptosis with an emphasis on its intricate connections to mitochondria and the basic components of cell death.