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Mitochondrial Redox Signaling during Apoptosis

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Abstract

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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  1. Department of Biochemistry, Emory University School of Medicine, Atlanta, GA, 30322

    Dean P. Jones

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  1. Jiyang Cai
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Cai, J., Jones, D.P. Mitochondrial Redox Signaling during Apoptosis. J Bioenerg Biomembr 31, 327–334 (1999). https://doi.org/10.1023/A:1005423818280

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