Can autophagy promote longevity?

Nat Cell Biol. 2010 Sep;12(9):842-6. doi: 10.1038/ncb0910-842.

Abstract

Organismal lifespan can be extended by genetic manipulation of cellular processes such as histone acetylation, the insulin/IGF-1 (insulin-like growth factor 1) pathway or the p53 system. Longevity-promoting regimens, including caloric restriction and inhibition of TOR with rapamycin, resveratrol or the natural polyamine spermidine, have been associated with autophagy (a cytoprotective self-digestive process) and in some cases were reported to require autophagy for their effects. We summarize recent developments that outline these links and hypothesize that clearing cellular damage by autophagy is a common denominator of many lifespan-extending manipulations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / physiology
  • Animals
  • Autophagy / drug effects
  • Autophagy / physiology*
  • Caenorhabditis elegans / physiology
  • Caloric Restriction
  • Cellular Senescence / physiology
  • Cytoprotection / physiology
  • Drosophila melanogaster / physiology
  • Humans
  • Immune System / physiology
  • Immunity / physiology
  • Longevity / drug effects
  • Longevity / physiology*
  • Mice
  • Receptor, IGF Type 1 / genetics
  • Resveratrol
  • Saccharomyces cerevisiae / physiology
  • Sirolimus / pharmacology
  • Sirtuin 1 / genetics
  • Spermidine / pharmacology
  • Stilbenes / pharmacology
  • Tumor Suppressor Protein p53 / genetics

Substances

  • Stilbenes
  • Tumor Suppressor Protein p53
  • Receptor, IGF Type 1
  • Sirtuin 1
  • Resveratrol
  • Spermidine
  • Sirolimus