Rejuvenation research最新文献

DNA damage represents one of the cell intrinsic causes of stem cell aging, which leads to differentiation-induced removal of damaged stem cells in skin and blood. Dietary restriction (DR) retards aging across various species, including several strains of laboratory mice. Whether, DR has the potential to ameliorate DNA damage-driven stem cell exhaustion remains incompletely understood. In this study, we show that DR strongly extends the time to hair graying in response to γ-irradiation (ionizing radiation [IR])-induced DNA damage of C57BL/6 J mice. The study shows that DR prolongs resting phase of hair follicles. DR-mediated prolongation of hair follicle stem cell (HFSC) quiescence blocks hair growth and prevents the depletion of HFSCs and ckit⁺ melanoblasts in response to IR. However, prolongation of HFSC quiescence also correlates with a suppression of DNA repair and cannot prevent melanoblast loss and hair graying in the long run, when hair cycling is reinitiated even after extended periods of time. Altogether, these results support a model indicating that nutrient deprivation can delay but not heal DNA damage-driven extinction of melanoblasts by stalling HFSCs in a prolonged state of quiescence coupled with inhibition of DNA repair. Disconnecting these two types of responses to DR could have the potential to delay stem cell aging.

This study aims to investigate the association between sleep duration and osteoporosis. In addition, sleep-related gene methylation was also detected in this study and we explored its relationship with osteoporosis. The epidemiological investigation section of this study was designed as a retrospective cross-sectional study. We gathered 148 postmenopausal women from two communities and used questionnaires to collect data of sleep duration and other sleep patterns. Biochemical variables were tested, and bone mineral density was measured by dual-energy X-ray absorptiometry. In addition, sleep-related gene (PER2 and PER3) methylation was tested, and the association with osteoporosis was further studied. Twenty-nine of the 148 participants (aged from 65 to 86 years) who suffered from osteoporosis were tested for osteopenia. A significant difference was observed in the association between sleep duration and osteoporosis; the p-value was 0.013. In addition, in our study, we found that short sleep duration (<7 hours) may increase the risk of osteoporosis compared with longer sleep duration. Moreover, sleep-related genes such as PER2 and PER3 and their CpG island methylation were tested, and there was no significant difference between PER2 and PER3 CpG island methylation and osteoporosis. Short sleep duration may increase the risk of osteoporosis. However, the association between sleep-related gene methylation and osteoporosis was not found.

Over 20 years ago, together with seven illustrious colleagues, the author proposed that efforts to postpone the decline and debilitation of aging might most promisingly be pursued by tackling the various lifelong processes of accumulation of damage through a panel of interventions, rather than seeking a magic bullet that would retard them all. A decade later, this approach was embraced in a paper that rapidly became, and is still, by far the most highly cited publication in the biology of aging this century. Here I survey the progress that the field has made in relation to this philosophy and the challenges that remain.