Mitochondrial outer-membrane permeabilization and remodelling in apoptosis.
Many human pathologies are associated with defects in mitochondria such as diabetes, neurodegenerative diseases or cancer. This tiny organelle is involved in a plethora of processes in mammalian cells, including energy production, lipid metabolism and cell death. In the so-called intrinsic apoptotic pathway, the outer mitochondrial membrane (MOM) is premeabilized by the pro-apoptotic Bcl-2 members Bax and Bak, allowing the release of apoptogenic factors such as cytochrome c from the inter-membrane space into the cytosol. At the same time, mitochondria fragment in response to Drp-1 activation suggesting that mitochondrial fission could play a role in mitochondrial outer-membrane permeabilization (MOMP). In this review, we will discuss the link that could exist between mitochondrial fission and fusion machinery, Bcl-2 family members and MOMP.
Department of Cell Biology, University of Geneva, Quai Ernest-Ansermet 30, 1211 Geneva 4, Switzerland.
Alexis
A
Jourdain
Jean-Claude
JC
Martinou
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D020558:GTP Phosphohydrolases / Q000378:metabolism / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D051336:Mitochondrial Membranes / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism / Q000502:physiology
D051028:bcl-2-Associated X Protein; D020558:GTP Phosphohydrolases