Mitochondrial dysfunction and cell senescence: cause or consequence?

João F Passos; Thomas von Zglinicki; Gabriele Saretzki

doi:10.1089/rej.2006.9.64

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Mitochondrial dysfunction and cell senescence: cause or consequence?

João F Passos·Thomas von Zglinicki·Gabriele Saretzki

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Abstract

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.

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Aging Cell Division Cellular Senescence Humans Mitochondria Oxidative Stress Reactive Oxygen Species Telomerase Telomere Journal Article Research Support, Non-U.S. Gov't Review

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João F Passos, Thomas von Zglinicki, Gabriele Saretzki. 2006. Mitochondrial dysfunction and cell senescence: cause or consequence?. https://doi.org/10.1089/rej.2006.9.64

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