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Mitochondria, telomeres and cell senescence

Lookup NU author(s): Dr Joao Passos, Professor Thomas von Zglinicki

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Abstract

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. © 2005 Elsevier Inc. All rights reserved.

Publication metadata

Author(s): Passos JF, Von Zglinicki T

Publication type: Note

Publication status: Published

Journal: Experimental Gerontology

Year: 2005

Volume: 40

Issue: 6

Pages: 466-472

ISSN (print): 0531-5565

ISSN (electronic): 1873-6815

URL: http://dx.doi.org/10.1016/j.exger.2005.04.006

DOI: 10.1016/j.exger.2005.04.006

PubMed id: 15963673

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