Mitochondrial Redox Signaling during Apoptosis

被引:0
作者
Jiyang Cai
Dean P. Jones
机构
[1] Emory University School of Medicine,Department of Biochemistry
来源
Journal of Bioenergetics and Biomembranes | 1999年 / 31卷
关键词
Apoptosis; redox; mitochondria; ROS; ASK-1; thioredoxin;
D O I
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中图分类号
学科分类号
摘要
The regulatory role of cellular redox state during apoptosis is still controversial. Early redoxsignaling can transduce divergent upstream signals to mitochondria and initiate apoptosis. Onthe other hand, release of mitochondrial cytochrome c triggers generation of reactive oxygenspecies (ROS) and renders apoptotic cells much more oxidized. Although the sequential caspaseactivation does not have apparent redox-sensitive components, redox signaling provides aseparate pathway that is parallel with the caspase cascade. The function of theapoptosis-associated redox change is uncertain. It could provide positive feedback mechanisms, such asactivating mitochondrial permeability transition and apoptosis signaling kinase (ASK-1). Sinceapoptotic cells are designated to be quickly eliminated, the dramatic cellular oxidation couldbe involved in the final degradation of apoptotic bodies and even the termination of theproteolytic activity after phagocytosis.
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页码:327 / 334
页数:7
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  • [1] Adams J. M.(1998)undefined Science 281 1322-1326
  • [2] Cory S.(1996)undefined Cell 87 171-306
  • [3] Alnemri E. S.(1998)undefined Cell Death Differ 5 298-475
  • [4] Livingston D. J.(1996)undefined J. Neurosci. Res. 43 465-8055
  • [5] Nicholson D. W.(1998)undefined J. Biol. Chem. 273 8048-716
  • [6] Salvesen G.(1973)undefined Biochem. J. 134 707-6364
  • [7] Thornberry N. A.(1998)undefined Mol. Cell. Biol. 18 6353-794
  • [8] Wong W. W.(1995)undefined Free Radical Biol. Med. 18 775-11404
  • [9] Yuan J.(1998)undefined J. Biol. Chem. 273 11401-966
  • [10] Amarante-Mendes G. P.(1999)undefined Invest. Ophthalmol. Visual Sci. 40 959-605