Cellular and Molecular Life Sciences

, Volume 67, Issue 10, pp 1589–1597

Mitochondrial control of caspase-dependent and -independent cell death

Authors

  • Ludivine A. Pradelli
    • Inserm, U895, Centre Méditerranéen de Médecine Moléculaire (C3M)
    • Université de Nice-Sophia-Antipolis, Faculté de Médecine
  • Marie Bénéteau
    • Inserm, U895, Centre Méditerranéen de Médecine Moléculaire (C3M)
    • Université de Nice-Sophia-Antipolis, Faculté de Médecine
    • Inserm, U895, Centre Méditerranéen de Médecine Moléculaire (C3M)
    • Université de Nice-Sophia-Antipolis, Faculté de Médecine
    • Centre Hospitalier Universitaire de Nice, Département d’Anesthésie Réanimation
Multi-author Review

DOI: 10.1007/s00018-010-0285-y

Cite this article as:
Pradelli, L.A., Bénéteau, M. & Ricci, J. Cell. Mol. Life Sci. (2010) 67: 1589. doi:10.1007/s00018-010-0285-y

Abstract

Mitochondria control whether a cell lives or dies. The role mitochondria play in deciding the fate of a cell was first identified in the mid-1990s, because mitochondria-enriched fractions were found to be necessary for activation of death proteases, the caspases, in a cell-free model of apoptotic cell death. Mitochondrial involvement in apoptosis was subsequently shown to be regulated by Bcl-2, a protein that was known to contribute to cancer in specific circumstances. The important role of mitochondria in promoting caspase activation has therefore been a major focus of apoptosis research; however, it is also clear that mitochondria contribute to cell death by caspase-independent mechanisms. In this review, we will highlight recent findings and discuss the mechanism underlying the mitochondrial control of apoptosis and caspase-independent cell death.

Keywords

MitochondriaBcl-2 familyCell deathApoptosisCaspase-independent cell deathMitochondrial outer membrane permeabilizationCancerBH3 mimetics

Copyright information

© Springer Basel AG 2010