氧化还原与细胞凋亡的关联

Redox signaling and apoptosis

细胞内氧化还原状态与细胞凋亡相互关联的机理仍然存在很大争议。细胞内氧化还原状态的改变促进了氧自由基(ROS)的产生和凋亡诱导因子的激活,致使细胞凋亡的同时又加剧了细胞内氧化还原状态的改变。通过激活细胞凋亡信号激酶(ASK-1)、氧化还原转录因子NF-kB、AP-1及Caspase激活,揭示了细胞内氧化还原状态伴随细胞凋亡的不同阶段。

The regulatory role of cellular redox state during apoptosis is still controversial. Redox signaling cantransduce signals upstream to mitochondria and initiate apoptosis. On the other hand, release of mitochondrialcytochrome C triggers generation of reactive oxygen species (ROS) and makes apoptotic cells much moreoxidized. 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 theapoptosis-associated redox change is uncertain. Some studies could provide positive feedback mechanisms,such as activating mitochondrial permeability transition, apoptosis signaling kinase (ASK-1) and redox-sensi-tive gene NF-kB. Simple redox signaling theory is difficult to explain how apoptosis happen,but each redoxsignaling plays a different role in the apoptosis process.