Lifestyle effects on telomeric shortening as a factor associated with biological aging: A systematic review

BACKGROUND: Telomeres are structures located at the chromosome ends, whose function is protecting DNA from attrition caused during cell division. Telomeric length serves as a mitotic clock, activating senescence and cellular cycle arrest when it reaches a shortening limit, which causes aging. Lifestyle is a factor that can affect telomeric shortening. Unhealthy habits have been linked to accelerated telomeric shortening, while healthy lifestyles are known to reduce this process and slow down aging. Current community has expressed an interest in improving lifestyle choices; however, an increase in unhealthy habits and chronic stressors have been seen. OBJECTIVE: This review aims to show the influence that different lifestyles have on telomeric length. METHODS: The review was carried out following the PRISMA statement in three databases. Twenty-eight research articles and nine review articles were reviewed, identifying six main lifestyles habits. RESULTS: Regular moderate-vigorous physical activity, dietary patterns rich in vegetables and antioxidants, and the stress control techniques were related to greater telomeric lengths and improvements in the oxidative response by reducing the levels of oxidative stress markers. On the contrary, stress, obesity, smoking, and alcoholism showed a negative effect of shorter telomeres, which can be a factor of early aging. CONCLUSION: The previous demonstrates the influences of lifestyles on telomere shortening rates and aging, therefore they should be considered as areas of interest for future research, and personal and community health improvement.

Nucleostemin prevents telomere damage by promoting PML-IV recruitment to SUMOylated TRF1

Continuously dividing cells must be protected from telomeric and nontelomeric DNA damage in order to maintain their proliferative potential. Here, we report a novel telomere-protecting mechanism regulated by nucleostemin (NS). NS depletion increased the number of telomere damage foci in both telomerase-active (TA+) and alternative lengthening of telomere (ALT) cells and decreased the percentage of damaged telomeres associated with ALT-associated PML bodies (APB) and the number of APB in ALT cells. Mechanistically, NS could promote the recruitment of PML-IV to SUMOylated TRF1 in TA+ and ALT cells. This event was stimulated by DNA damage. Supporting the importance of NS and PML-IV in telomere protection, we demonstrate that loss of NS or PML-IV increased the frequency of telomere damage and aberration, reduced telomeric length, and perturbed the TRF2ΔBΔM-induced telomeric recruitment of RAD51. Conversely, overexpression of either NS or PML-IV protected ALT and TA+ cells from telomere damage. This work reveals a novel mechanism in telomere protection.