Mitochondrial dysfunction and cell senescence: cause or consequence?
The mitochondrial theory of aging remains to date one of the most popular theories of aging. One major model of aging is replicative senescence, where the irreversible loss of division potential of somatic cells occurs after a more or less constant number of cell divisions. Few data are available concerning the role of mitochondria in this model. Here, we review evidence supporting the involvement of mitochondria in replicative senescence and a possible link to telomere biology. Moreover, we suggest that this process might be more complex than originally formulated, because variations in nuclear gene expression involved in mitochondrion nucleus cross-talk are observed in both senescence and immortalization.
Passos
João F
JF
Henry Wellcome Laboratory for Biogerontology Research, Institute for Aging and Health, University of Newcastle, Newcastle upon Tyne, United Kingdom. Joao.Passos@ncl.ac.uk
von Zglinicki
Thomas
T
Saretzki
Gabriele
G
D000375:Aging / Q000502:physiology*; D002455:Cell Division; D016922:Cellular Senescence / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D019098:Telomerase / Q000378:metabolism; D016615:Telomere / Q000502:physiology
D017382:Reactive Oxygen Species; D019098:Telomerase