Investigation of the regression of advanced atherosclerosis through the regulation of cellular senescence-custom-made therapy to Japanese elderly-

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Aging is associated with diabetes and dyslipidemia as atherosclerosis characterized by endothelial dysfunction and oxidative stress leading NO destruction. We introduce one example. High glucose especially causes stress-induced premature and replicative senescence. We examined the regulatory role of various products on NO bioavailability, endothelial senescence and its functions. Exposure of HUVECs to high glucose for increased SA-βgalactosidase activity, a senescence marker, and decreased telomerase activity, a replicative senescence marker. We found the anti-senescent effect of statin, estrogen and citrulline. eNOSsiRNA reduced those effects. Streptozotocin-induced diabetes showed more senescent cells in endothelium of aged rats compared with age-matched control and insulin, statin or estrogen-treated rats. The regulatory effects of various products on endothelial senescence might be important for elderly medicine.