Age to survive: DNA damage and aging.
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.
Schumacher
Björn
B
MGC Department of Cell Biology and Genetics, Center for Biomedical Genetics, Erasmus Medical Center, 3000 DR Rotterdam, The Netherlands.
Garinis
George A
GA
Hoeijmakers
Jan H J
JH
D000375:Aging / Q000235:genetics* / Q000378:metabolism*; D000818:Animals; D003057:Cockayne Syndrome / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D004195:Disease Models, Animal; D019143:Evolution, Molecular; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007448:Invertebrates; D008136:Longevity; D051379:Mice; D009369:Neoplasms / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D011371:Progeria / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
D025521:Tumor Suppressor Proteins; D007334:Insulin-Like Growth Factor I