Pathomechanisms of Photoaged Skin

Abstract

Among all environmental factors, solar UV radiation is the most important in premature skin aging, a process accordingly termed photoaging. Over recent years, substantial progress has been made in elucidating the underlying molecular mechanisms. From these studies, it is now clear that both UVB (290–320 nm) and UVA (320– 400 nm) radiations contribute to photoaging. UVinduced alterations at the level of the dermis are best studied and appear to be largely responsible for the phenotype of photoaged skin. It is also generally agreed that UVB acts preferentially on the epidermis where it not only damages DNA in keratinocytes and melanocytes, but also causes the production of soluble factors including proteolytic enzymes, which in a second step affect the dermis; in contrast, UVA radiation penetrates far more deeply on average and hence exerts direct effects on both the epidermal and the dermal compartments (> Fig. 10.1). UVA is also 10–100 times more abundant in sunlight than UVB, depending on the season and time of the day. Therefore, it has been proposed that, although UVA photons are individually far less biologically active than UVB photons, UVA radiation may be at least as important as UVB radiation in the pathogenesis of photoaging [1]. The exact mechanisms by which UV radiation causes premature skin aging is not yet clear, but a number of molecular pathways explaining one or more of the key features of photoaged skin have been described. Some of these models are based on irradiation protocols, which use single or few UV exposures, whereas others take into account the fact that photoaging results from chronic UV damage, and as a consequence employ chronic repetitive irradiation protocols. Still others rely on largely theoretical constructs rather than experimental observations.