Mitochondria, telomeres and cell senescence

João F. Passos, Thomas Von Zglinicki

Research output: Contribution to journalShort surveypeer-review

94 Scopus citations


The accumulation of oxidative damage is one of the most widely accepted causes of ageing. Mitochondrial dysfunction, in particular damage to the mitochondrial DNA has been hypothesised, more than thirty years ago, as responsible for increased production of reactive oxygen species (ROS) and, thus, as one possible causal factor for ageing. There is now a wealth of data that supports this hypothesis, which is mostly derived from models considering the ageing of post-mitotic or slowly dividing cells in vivo. One major cellular model of ageing, however, is replicative senescence, the irreversible loss of division potential of somatic cells after a more or less constant number of cell divisions. Not much data exists concerning the role of mitochondria in this model. Here, we review evidence supporting an involvement of mitochondria in replicative senescence and a possible link to telomere shortening.

Original languageEnglish (US)
Pages (from-to)466-472
Number of pages7
JournalExperimental Gerontology
Issue number6
StatePublished - Jun 2005


  • Fibroblasts
  • Mitochondria
  • Oxidative stress
  • Senescence
  • Telomeres
  • Uncoupling

ASJC Scopus subject areas

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


Dive into the research topics of 'Mitochondria, telomeres and cell senescence'. Together they form a unique fingerprint.

Cite this