[Autophagy in cell survival and death].
Macroautophagy hereafter referred to as autophagy is a major lysosomal catabolic pathway for macromolecules and organelles conserved in eukaryotic cells. The discovery of the molecular basis of autophagy has uncovered its importance during development, life extension and in pathologies such as cancer, certain forms of myopathies and neurodegenerative diseases. Autophagy is a cell survival mechanism during starvation that is controlled by amino acids. Starvation-induced autophagy is an anti-apoptotic mechanism. However autophagy is also an alternative to apoptosis through autophagic cell death. In many situations apoptosis and autophagy can both contribute to cell dismantlement.
INSERM U504, Institut André Lwoff Université Paris XI, 16, avenue Paul-Vaillant-Couturier, 94807 Villejuif Cedex. codogno@vjf.inserm.fr
Patrice
P
Codogno
D000596:Amino Acids / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001343:Autophagy / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology*; D005057:Eukaryotic Cells / Q000166:cytology; D006728:Hormones / Q000502:physiology; D006801:Humans; D008247:Lysosomes / Q000502:physiology; D008928:Mitochondria / Q000502:physiology; D008954:Models, Biological; D009135:Muscular Diseases / Q000473:pathology; D009369:Neoplasms / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D011494:Protein Kinases / Q000502:physiology; D013217:Starvation / Q000503:physiopathology; D058570:TOR Serine-Threonine Kinases
D000596:Amino Acids; D006728:Hormones; D019869:Phosphatidylinositol 3-Kinases; D011494:Protein Kinases; D058570:TOR Serine-Threonine Kinases; C546842:MTOR protein, human