Revista de Dermatologia e Doenças Dermatológicas

The fight against aging, which is defined as a set of physiological mechanisms that alter the physical and intellectual capacities of humans, is one of the major challenges of the 21^st century. This process includes more than just skin aging. Major healing defects are linked in part to changes in the biomechanical properties of skin cells, primarily dermal fibroblasts, that are associated with this condition. The immune system, which is also crucial for wound healing and maintaining skin homeostasis, is affected by time as well:Skin immunosenescence would result, promoting a pro-tumor environment while limiting the anti-infectious and vaccine responses. Before listing the effective anti-aging strategies to combat age-related dermal and epidermal stigmas, the primary skin damages caused by aging— whether intrinsic or extrinsic—will be discussed in detail.

White spots on the skin are the result of melanocytes being destroyed by CD8+ T cells in the autoimmune condition known as vitiligo. Numerous studies indicate that oxidative stress is a significant contributor to the onset of vitiligo from the very beginning. Overproduction of reactive oxygen species (ROS) and ROS accumulation in vulnerable melanocytes are jointly caused by multiple factors. ROS, on the other hand, play a role in the production of autoantigens and melanocyte damage at the level of molecules, organelles and cells through a variety of pathways connected to melanocyte dysregulation. Autoantigen presentation is mediated by innate immunity, which acts as a bridge between adaptive immunity and oxidative stress, according to recent research. The final destruction of epidermal melanocytes is guaranteed by the recruitment of CD8+ T cells induced by cytokines and chemokines. In addition, the reinstatement and relapse of vitiligo can be explained by emerging concerns regarding resident memory T cells and regulatory T cells. In this article, we attempt to uncover additional connections between autoimmunity and oxidative stress, as well as new perspectives on recent developments in our knowledge of the disease's pathogenesis.