Aging represents the progressive functional decline and increased mortality risk common to nearly all metazoans. Recent findings experimentally link DNA damage and organismal aging: longevity-regulating genetic pathways respond to the accumulation of DNA damage and other stress conditions and conversely influence the rate of damage accumulation and its impact for cancer and aging. This novel insight has emerged from studies on human progeroid diseases and mouse models that have deficient DNA repair pathways. Here we discuss a unified concept of an evolutionarily conserved 'survival' response that shifts the organism's resources from growth to maintenance as an adaptation to stresses, such as starvation and DNA damage. This shift protects the organism from cancer and promotes healthy aging.

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Persistent URL dx.doi.org/10.1016/j.tig.2007.11.004, hdl.handle.net/1765/29313
Citation
Schumacher, B, Garinis, G.A, & Hoeijmakers, J.H.J. (2008). Age to survive: DNA damage and aging. Trends in Genetics, 24(2), 77–85. doi:10.1016/j.tig.2007.11.004