Increased age-adjusted hazard of death associated with a common single nucleotide polymorphism of the human RAD52 gene in a cardiovascular cohort
| Authors | |
|---|---|
| Year of publication | 2017 |
| Type | Article in Periodical |
| Magazine / Source | Mechanisms of Ageing and Development |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.1016/j.mad.2017.10.003 |
| Field | Physiology |
| Keywords | Aging; DNA damage; DNA damage response; Double strand breaks; Longitudinal study; RAD52 |
| Description | Aging may be characterized as the progressive increase of the risk of death caused by a decrease of almost all bodily functions. While a great number of model organism studies have established the role of DNA double strand breaks (DSBs) as one of the main causes of aging, few studies have examined whether common polymorphisms in human DSB repair genes influence aging and mortality. More importantly, to the best of our knowledge, no longitudinal study has thus far examined the link between polymorphisms in DSB repair and the risk of death. This longitudinal study thus analyses whether four common polymorphisms (rs2155209, rs7963551, rs17105278, rs2735383) in four selected DSB repair genes (MRE11A, RAD52, RAD51B, NBS1) influence the hazard of age-adjusted death in a cohort of patients with typical symptoms of ischemic heart disease. The results have shown that rs7963551 G/T heterozygotes exhibit a significantly increased hazard of death when compared with the combined GG and TT homozygotes (HR = 1.42, 95% CI: 1.06–1.91, p = 0.018). This study indicates that the SNP affecting efficiency of DSB repair may influence aging in humans. |
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