Neuronal survival and cell death signaling pathways

Adv Exp Med Biol. 2002:513:41-86. doi: 10.1007/978-1-4615-0123-7_2.

Abstract

Neuronal viability is maintained through a complex interacting network of signaling pathways that can be perturbed in response to a multitude of cellular stresses. A shift in the balance of signaling pathways after stress or in response to pathology can have drastic consequences for the function or the fate of a neuron. There is significant evidence that acutely injured and degenerating neurons may die by an active mechanism of cell death. This process involves the activation of discrete signaling pathways that ultimately compromise mitochondrial structure, energy metabolism and nuclear integrity. In this review we examine recent evidence pertaining to the presence and activation of anti- and pro-cell death regulatory pathways in nervous system injury and degeneration.

Publication types

  • Review

MeSH terms

  • Calpain / metabolism
  • Caspase Inhibitors
  • Caspases / metabolism
  • Cell Death / physiology*
  • Cell Nucleus / metabolism
  • Cell Survival / physiology*
  • DNA Damage
  • Glycogen Synthase Kinase 3 / metabolism
  • Glycogen Synthase Kinase 3 beta
  • MAP Kinase Signaling System / physiology*
  • Mitochondria / metabolism
  • Neurons / physiology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor / metabolism
  • Receptors, Tumor Necrosis Factor / metabolism
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Caspase Inhibitors
  • Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor
  • Receptors, Tumor Necrosis Factor
  • Tumor Suppressor Protein p53
  • Glycogen Synthase Kinase 3 beta
  • Protein Serine-Threonine Kinases
  • Glycogen Synthase Kinase 3
  • Calpain
  • Caspases