Mitochondrial dysfunction and longevity in animals: Untangling the knot

Science. 2015 Dec 4;350(6265):1204-7. doi: 10.1126/science.aac4357.

Abstract

Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity.

Publication types

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

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Animals
  • Caenorhabditis elegans Proteins / genetics
  • Electron Transport / genetics
  • Electron Transport Complex III / genetics
  • Longevity / genetics
  • Longevity / physiology*
  • Mice
  • Mice, Knockout
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Point Mutation
  • Reactive Oxygen Species / metabolism*

Substances

  • Caenorhabditis elegans Proteins
  • Reactive Oxygen Species
  • Adenosine Triphosphate
  • Isp-1 protein, Caenorhabditis elegans
  • Electron Transport Complex III