The paradox of mitochondrial dysfunction and extended longevity

Erin Munkácsy, Shane L. Rea

Research output: Contribution to journalReview articlepeer-review

70 Scopus citations


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
StatePublished - Aug 2014


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

ASJC Scopus subject areas

  • Biochemistry
  • Aging
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology


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