RESUMO
Vitamin D is considered an essential micronutrient for human health that is metabolized into a multifunctional secosteroid hormone. We can synthesize it in the skin through ultraviolet B (UVB) rays or acquire it from the diet. Its deficiency is a major global health problem that affects all ages and ethnic groups. Furthermore, dysregulation of vitamin D homeostasis has been associated with premature aging, driven by various cellular processes, including oxidative stress and cellular senescence. Various studies have shown that vitamin D can attenuate oxidative stress and delay cellular senescence, mainly by inducing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and Klotho and improving mitochondrial homeostasis, proposing this vitamin as an excellent candidate for delaying aging. However, the mechanisms around these processes are not yet fully explored. Therefore, in this review, the effects of vitamin D on redox regulation and cellular senescence are discussed to propose new lines of research and clinical applications of vitamin D in the context of age-related diseases.