By José Marín-García; Michael J Goldenthal; Gordon W Moe
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Mitochondrial DNA involvement in human longevity. Biochim Biophys Acta 2006;1757:1388–1399 28. Heijmans BT, Westendorp RG, Knook DL, Kluft C, Slagboom PE. Angiotensin I-converting enzyme and plasminogen activator inhibitor-1 gene variants: risk of mortality and fatal cardiovascular disease in an elderly population-based cohort. J Am Coll Cardiol 1999;34:1176–1183 29. Juhan-Vague I, Pyke SM, Alessi MC, Jespersen J, Haverkate F, Thompson SG. Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris.
This sustained life-long reduction in mortality rate suggests that the effect is due to genetic rather than environmental or socio-economic factors. Another study supported the idea that exceptional longevity has a genetic component by using a genome-wide scan of 308 individuals belonging to 137 sibships demonstrating exceptional longevity to identify a locus on chromosome 4 that exhibited significant linkage with exceptional longevity and therefore is likely to contain gene(s) that promote longevity .
Molecules that may have a significant role in the repair of telomeric DNA prior to replicative senescence include ATM, p53, PARP, DNA-PK, Ku70/80, the human hRad50-hMre11-p95 complex, BRCA 1 and 2 and the helicases that are implicated in Bloom’s and Werner’s syndrome. Fig. 3 The correlation of oxidative stress, telomeric damage and cell senescence with premature aging, normal aging and increased longevity. 24 Post-Genomic View of Aging: Definitions, Theories and Observations As observed by Stewart and Weinberg , the cell phenotype of senescence operates to circumscribe the proliferative potential of mammalian cells, and the key regulators of these phenotypes are the telomeres whose erosion below a certain length can trigger crisis.