Mitochondrial redox signaling during apoptosis

Jiyang Cai, Dean P. Jones

Research output: Contribution to journalArticle

95 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)327-334
Number of pages8
JournalJournal of Bioenergetics and Biomembranes
Volume31
Issue number4
DOIs
StatePublished - 1999
Externally publishedYes

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Keywords

  • Apoptosis
  • ASK-I
  • E(h), ROS
  • Mitochondria
  • Redox
  • Thioredoxin

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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