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FEBS Lett. 1996 Oct 28;396(1):7-13.

Mitochondria and programmed cell death: back to the future.

Author information

1
Centre de Génétique Moléculaire, CNRS UPR 2420, Gif-sur-Yvette, France. petitpx@cgm.cnrs-gif.fr

Abstract

Programmed cell death, or apoptosis, has in the past few years undoubtedly become one of the most intensively investigated biological processes. However, fundamental questions concerning the molecular and biochemical mechanisms remain to be elucidated. The central question concerns the biochemical steps shared by the numerous death induction pathways elicited by different stimuli. Heterogeneous death signals precede a common effector phase during which cells pass a threshold of 'no return' and are engaged in a degradation phase where they acquire the typical onset of late apoptosis. Alterations in mitochondrial permeability transition linked to membrane potential disruption precede nuclear and plasma membrane changes. In vitro induction of permeability transition in isolated mitochondria provokes the release of a protein factor capable of inducing nuclear chromatin condensation and fragmentation. This permeability transition is regulated by multiple endogenous effectors, including members of the bcl-2 gene family. Inhibition of these effects prevents apoptosis.

PMID:
8906857
DOI:
10.1016/0014-5793(96)00988-x
[Indexed for MEDLINE]
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