The paradox of mitochondrial dysfunction and extended longevity

Erin Munkácsy, Shane L. Rea

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Mitochondria play numerous, essential roles in the life of eukaryotes. Disruption of mitochondrial function in humans is often pathological or even lethal. Surprisingly, in some organisms mitochondrial dysfunction can result in life extension. This paradox has been studied most extensively in the long-lived Mit mutants of the nematode Caenorhabditis elegans. In this review, we explore the major responses that are activated following mitochondrial dysfunction in these animals and how these responses potentially act to extend their life. We focus our attention on five broad areas of current research - reactive oxygen species signaling, the mitochondrial unfolded protein response, autophagy, metabolic adaptation, and the roles played by various transcription factors. Lastly, we also examine why disruption of complexes I and II differ in their ability to induce the Mit phenotype and extend lifespan.

Original languageEnglish (US)
Pages (from-to)221-233
Number of pages13
JournalExperimental Gerontology
Volume56
DOIs
StatePublished - 2014

Fingerprint

Mitochondria
Reactive Oxygen Species
Animals
Transcription Factors
Unfolded Protein Response
Mitochondrial Proteins
Autophagy
Caenorhabditis elegans
Life Expectancy
Eukaryota
Proteins
Phenotype
Research

Keywords

  • Aging
  • C. elegans
  • Lifespan
  • Metabolism
  • Mit mutant
  • Mitochondria

ASJC Scopus subject areas

  • Aging
  • Biochemistry
  • Cell Biology
  • Endocrinology
  • Genetics
  • Molecular Biology
  • Medicine(all)

Cite this

The paradox of mitochondrial dysfunction and extended longevity. / Munkácsy, Erin; Rea, Shane L.

In: Experimental Gerontology, Vol. 56, 2014, p. 221-233.

Research output: Contribution to journalArticle

Munkácsy, Erin ; Rea, Shane L. / The paradox of mitochondrial dysfunction and extended longevity. In: Experimental Gerontology. 2014 ; Vol. 56. pp. 221-233.
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