Nucleic Acids Research Advance Access originally published online on October 2, 2007
Nucleic Acids Research 2007 35(22):7417-7428; doi:10.1093/nar/gkm681
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Nucleic Acids Research, 2007, Vol. 35, No. 22 7417-7428
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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DNA damage, cellular senescence and organismal ageing: causal or correlative?
Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QR, UK
*To whom correspondence should be addressed. Tel: +44 (0)1223 336784; Fax: +44 (0)1223 330598; Email: jhc36{at}cam.ac.uk
Received July 2, 2007. Revised August 16, 2007. Accepted August 17, 2007.
Cellular senescence has long been used as a cellular model for understanding mechanisms underlying the ageing process. Compelling evidence obtained in recent years demonstrate that DNA damage is a common mediator for both replicative senescence, which is triggered by telomere shortening, and premature cellular senescence induced by various stressors such as oncogenic stress and oxidative stress. Extensive observations suggest that DNA damage accumulates with age and that this may be due to an increase in production of reactive oxygen species (ROS) and a decline in DNA repair capacity with age. Mutation or disrupted expression of genes that increase DNA damage often result in premature ageing. In contrast, interventions that enhance resistance to oxidative stress and attenuate DNA damage contribute towards longevity. This evidence suggests that genomic instability plays a causative role in the ageing process. However, conflicting findings exist which indicate that ROS production and oxidative damage levels of macromolecules including DNA do not always correlate with lifespan in model animals. Here we review the recent advances in addressing the role of DNA damage in cellular senescence and organismal ageing.
Deceased.
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