[Apoptosis: molecular mechanisms].
Apoptosis is a genetically programmed cell death that is required for morphogenesis during embryogenic development and for tissue homeostasis in adult organisms. In most cases, apoptosis involves cytochrome c release from mitochondria. In the cytosol, cytochrome c combines with APAF-1 in the presence of ATP to activate caspase-9 that, in turn, activates effectors caspases such as caspase-3. Bcl-2 and related proteins control cytochrome c release from the mitochondria whereas IAP (for Inhibitor of APoptosis) molecules modulate the activity of caspases. Plasma membrane receptors such as Fas (CD95, APO-1), characterized by a so-called "death domain" in their cytoplasmic domain, can activate the caspase cascade through adaptator molecules such as FADD (Fas-Associated protein with a Death Domain). Dysregulation of the apoptotic machinery plays a role in the pathogenesis of various diseases and molecules involved in cell death pathways are potential therapeutic targets in immunologic, neurologic, cancer, infectious and inflammatory diseases.
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Unité INSERM 517 Mort cellulaire et cancer, Facultés de Médecine et de Pharmacie, Dijon. esolary@u-bourgogne.fr
D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D005314:Embryonic and Fetal Development; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D009024:Morphogenesis