Cytochrome C-mediated apoptosis

Annu Rev Biochem. 2004;73:87-106. doi: 10.1146/annurev.biochem.73.011303.073706.

Abstract

Apoptosis, or programmed cell death, is involved in development, elimination of damaged cells, and maintenance of cell homeostasis. Deregulation of apoptosis may cause diseases, such as cancers, immune diseases, and neurodegenerative disorders. Apoptosis is executed by a subfamily of cysteine proteases known as caspases. In mammalian cells, a major caspase activation pathway is the cytochrome c-initiated pathway. In this pathway, a variety of apoptotic stimuli cause cytochrome c release from mitochondria, which in turn induces a series of biochemical reactions that result in caspase activation and subsequent cell death. In this review, we focus on the recent progress in understanding the biochemical mechanisms and regulation of the pathway, the roles of the pathway in physiology and disease, and their potential therapeutic values.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Caenorhabditis elegans / cytology
  • Caenorhabditis elegans / metabolism
  • Caspases / metabolism
  • Cytochromes c / metabolism*
  • Enzyme Activation
  • Humans
  • Mitochondria / metabolism
  • Models, Biological
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Receptors, Tumor Necrosis Factor / metabolism

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Receptors, Tumor Necrosis Factor
  • Cytochromes c
  • Caspases