Abstract
Aging is a central risk factor for many age-related pathologies including cancer, cardiovascular disease, and autoimmune disease. Therefore, a mechanistic understanding of the aging process promises great potential for discoveries of therapeutic measures that can relieve the burden of age-related pathologies. According to the “DNA damage–accumulation theory of aging,” the accumulation of unrepaired DNA damage and resulting genomic instability play a central role in promoting aging. In line with this, numerous DNA-repair diseases are characterized by increased genomic instability and recapitulation of several symptoms of normal aging. Numerous intrinsic and extrinsic factors contribute to age-dependent DNA-damage accumulation, including oxidative stress, DNA-replication errors, deteriorating genome-maintenance mechanisms, altered nuclear organization, and survival in the presence of DNA damage. This negatively affects cell and tissue homeostasis through causing changes in gene-expression profiles, or inducing cellular senescence or apoptosis, thereby promoting functional decline of tissue function, which is characteristic for aging.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have