摘要：Aging is the accumulation of unrepaired damage to cellular and organismal components over time. Damage to nuclear DNA likely contributes to the degenerative effects of aging; unlike other cellular constituents, nuclear DNA cannot be replaced [1]. A wide spectrum of DNA lesions and associated repair pathways exist [1]: non-helix distorting lesions, such as those induced by oxidative damage, are repaired via base excision repair (BER); whereas helix-distorting base changes, like those caused by UV, are fixed via nucleotide excision repair (NER) and its subpathways. DNA double strand breaks (DSBs) represent a particularly severe challenge to the cell; if left unrepaired these lesions can induce cell death, replicative senescence, or conversely promote oncogenic transformation. For this reason, cells have evolved multiple pathways to repair DSBs: classical non-homologous end-joining (C-NHEJ), homologous recombination (HR), and other pathways such as alternative NHEJ [2,3,4]. In this issue of Aging, workby Chua, McCord et al. suggests that SIRT6, a member of a protein family previously implicated in promoting longevity, may function at least in part via increasing efficacy of DNA repair.
