Uncoupling protein-2 regulates lifespan in mice

Am J Physiol Endocrinol Metab. 2009 Apr;296(4):E621-7. doi: 10.1152/ajpendo.90903.2008. Epub 2009 Jan 13.

Abstract

The long-term effects of uncoupled mitochondrial respiration by uncoupling protein-2 (UCP2) in mammalian physiology remain controversial. Here we show that increased mitochondrial uncoupling activity of different tissues predicts longer lifespan of rats compared with mice. UCP2 reduces reactive oxygen species (ROS) production and oxidative stress throughout the aging process in different tissues in mice. The absence of UCP2 shortens lifespan in wild-type mice, and the level of UCP2 positively correlates with the postnatal survival of superoxide dismutase-2 mutant animals. Thus UCP2 has a beneficial influence on cell and tissue function leading to increased lifespan.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ion Channels / genetics
  • Ion Channels / physiology*
  • Longevity / genetics*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / physiology*
  • Oxidative Stress / genetics
  • Oxygen Consumption / genetics
  • Rats
  • Rats, Inbred F344
  • Reactive Oxygen Species / metabolism
  • Respiration / genetics
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / physiology
  • Survival Analysis
  • Uncoupling Protein 2

Substances

  • Ion Channels
  • Mitochondrial Proteins
  • Reactive Oxygen Species
  • Ucp2 protein, mouse
  • Ucp2 protein, rat
  • Uncoupling Protein 2
  • Superoxide Dismutase
  • superoxide dismutase 2