The Plasticity of Aging: Insights From Long-Lived Mutants

Cell. 2005 Feb 25;120(4):449-60. doi: 10.1016/j.cell.2005.02.002.

Abstract

Mutations in genes affecting endocrine signaling, stress responses, metabolism, and telomeres can all increase the life spans of model organisms. These mutations have revealed evolutionarily conserved pathways for aging, some of which appear to extend life span in response to sensory cues, caloric restriction, or stress. Many mutations affecting longevity pathways delay age-related disease, and the molecular analysis of these pathways is leading to a mechanistic understanding of how these two processes--aging and disease susceptibility--are linked.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Evolution
  • Disease Susceptibility
  • Insulin / genetics
  • Insulin / physiology
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / physiology
  • Longevity / genetics*
  • Longevity / physiology
  • Mitochondria / genetics*
  • Mitochondria / physiology
  • Mutation* / physiology
  • Oxidative Stress / genetics
  • Oxidative Stress / physiology
  • Reproduction / genetics*
  • Reproduction / physiology
  • Telomere / genetics*
  • Telomere / physiology

Substances

  • Insulin
  • Insulin-Like Growth Factor I