Characteristics and Pathomechanisms of Endogenously Aged Skin

Abstract

The skin, being in direct contact with several environmental factors (e.g. UV irradiation), does not only undergo endogenous aging, which has to do with the ‘biological clock’ of the skin cells per se, but also exogenous aging. While exogenous skin aging has been extensively studied, the pathomechanisms of endogenous skin aging remain far less clear. Endogenous skin aging reflects reduction processes, which are common in internal organs. These processes include cellular senescence and decreased proliferative capacity, decrease in cellular DNA repair capacity and chromosomal abnormalities, loss of telomeres, point mutations of extranuclear mtDNA, oxidative stress and gene mutations. As a consequence, aged skin in nonexposed areas shows typical characteristics including fine wrinkles, dryness, sallowness and loss of elasticity. Recent data have illustrated that lack of hormones occurring with age may also contribute to the aging phenotype. Improvement of epidermal skin moisture, elasticity and skin thickness, enhanced production of surface lipids, reduction of wrinkle depth, restoration of collagen fibers and increase of the collagen III/I ratio have been reported after hormone replacement therapy or local estrogen treatment in postmenopausal women. Furthermore, an in vitro model of endogenous skin aging consisting of human SZ95 sebocytes which were incubated under a hormone-substituted environment illustrated that hormones at age- and sex-specific levels were able to alter the development of cells by regulating their transcriptome. In conclusion, among other factors the hormone environment plays a distinct role in the generation of aged skin.