Mitochondria, reactive oxygen species, and chronological aging: a message from yeast

Exp Gerontol. 2011 Nov;46(11):847-52. doi: 10.1016/j.exger.2011.08.007. Epub 2011 Aug 22.

Abstract

As a major intracellular source of reactive oxygen species (ROS), mitochondria are involved in aging and lifespan regulation. Using the yeast chronological aging model, researchers have identified conserved signaling pathways that affect lifespan by modulating mitochondrial functions. Caloric restriction and a genetic mimetic with reduced target of rapamycin signaling globally upregulate the mitochondrial proteome and respiratory functions. Recent discoveries support the notion that an altered mitochondrial proteome induces mitohormesis. Mitohormesis involves a variety of ROS during several growth stages and extends lifespan in yeast and other organisms. Here we recap recent advances in understanding of ROS as signals that decelerate chronological aging in yeast. We also discuss parallels between yeast and worm hypoxic signaling. In sum, this mini-review covers mitochondrial regulation by nutrient-sensing pathways and the complex underlying interactions of ROS, metabolic pathways, and chronological aging.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Aging / drug effects
  • Aging / metabolism*
  • Animals
  • Caloric Restriction
  • Cell Hypoxia / drug effects
  • Humans
  • Longevity
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • Oxidative Stress / physiology*
  • Protein-Serine-Threonine Kinases / metabolism*
  • Proteome
  • Reactive Oxygen Species / metabolism*
  • Saccharomyces cerevisiae Proteins / metabolism*
  • Signal Transduction
  • Up-Regulation
  • Yeasts / drug effects
  • Yeasts / metabolism*

Substances

  • Proteome
  • Reactive Oxygen Species
  • Saccharomyces cerevisiae Proteins
  • Protein-Serine-Threonine Kinases
  • target of rapamycin protein, S cerevisiae