Connecting autophagy to senescence in pathophysiology

Curr Opin Cell Biol. 2010 Apr;22(2):234-40. doi: 10.1016/j.ceb.2009.12.005. Epub 2010 Jan 4.

Abstract

Cellular senescence is an extremely stable form of cell cycle arrest activated in response to stress. Autophagy, a lysosome-dependent cellular catabolic process, can also be triggered by cellular stresses. Both senescence and autophagy have been implicated in a similar range of pathophysiologies, including cancer, aging and age-related symptoms. Senescence is a heterogeneous phenotype that is composed of multiple effector mechanisms and autophagy was recently identified as a new effector of senescence. Autophagy seemingly has different impacts on cells responding to stress through a diversity of effects: recycling of metabolic waste, cell survival and protein expression regulation.

MeSH terms

  • Animals
  • Autophagy*
  • Cellular Senescence*
  • Disease*
  • Feedback, Physiological
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Phenotype
  • Protein-Serine-Threonine Kinases / metabolism
  • TOR Serine-Threonine Kinases
  • beta-Galactosidase / metabolism

Substances

  • Intracellular Signaling Peptides and Proteins
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • Protein-Serine-Threonine Kinases
  • beta-Galactosidase