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Due to its ability to cross the epidermis and reach the upper dermis where it causes cumulative DNA damage and increased oxidative stress, UVB is considered the most harmful component of sunlight to the skin. The consequences of chronic exposition to UVB are related to photoaging and photocarcinogenesis. There are limitations to the study of human skin aging and for this reason the use of models is required. Human dermal fibroblasts submitted to mild and repeated doses of UVB are considered a versatile model to study UVB effects in the process of skin photoaging, which depends on the accumulation of senescent cells, in particular in the dermis. Here we provide updated information about the current model of UVB-induced senescence with special emphasis on the process of protein quality control.Senescent cells accumulate in the skin during aging.UVB-induced senescence of fibroblasts contributes to overall skin photoaging.UVB treatment leads to cell cycle arrest and activation of many signaling pathways.UVB irradiation leads to increased ROS and impairment of proteasome activity.In this system autophagy is crucial for the development of the senescent phenotype.