[The two faces of autophagy in the nervous system]

Med Sci (Paris). 2009 Apr;25(4):383-90. doi: 10.1051/medsci/2009254383.
[Article in French]

Abstract

Autophagy is a cellular mechanism for degrading proteins and organelles. It was first described as a physiological process essential for maintaining homeostasis and cell survival, but understanding its role in conditions of stress has been complicated by the recognition of a new type of cell death ("type 2") characterized by deleterious autophagic activity. This paradox is important in the central nervous system where the activation of autophagy seems to be protective in certain neurodegenerative diseases but deleterious in cerebral ischemia. The development of new therapeutic strategies based on the manipulation of autophagy will need to take into account these opposing roles of autophagy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autophagy / genetics
  • Autophagy / physiology*
  • Brain Ischemia / pathology
  • Brain Ischemia / physiopathology*
  • Chick Embryo
  • Embryonic Development
  • Humans
  • Larva / growth & development
  • Lysosomes / physiology
  • Mammals / genetics
  • Mammals / physiology
  • Models, Biological
  • Molecular Chaperones / physiology
  • Multiprotein Complexes / physiology
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / physiology
  • Nervous System Physiological Phenomena*
  • Neurodegenerative Diseases / physiopathology*
  • Phosphatidylinositol 3-Kinases / physiology
  • Protein Kinases / physiology
  • Ranidae / growth & development
  • Receptors, N-Methyl-D-Aspartate / agonists
  • Receptors, N-Methyl-D-Aspartate / physiology
  • TOR Serine-Threonine Kinases

Substances

  • Molecular Chaperones
  • Multiprotein Complexes
  • Nerve Tissue Proteins
  • Receptors, N-Methyl-D-Aspartate
  • Protein Kinases
  • MTOR protein, human
  • TOR Serine-Threonine Kinases