Makrantonaki Evgenia, Zouboulis Christos C
Laboratory for Biogerontology, Dermato-Pharmacology and Dermato-Endocrinology, Institute of Clinical Pharmacology and Toxicology, Charité Universitatsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
Dermatology. 2007;214(4):352-60. doi: 10.1159/000100890.
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.
皮肤与多种环境因素（如紫外线照射）直接接触，不仅会经历与皮肤细胞自身“生物钟”相关的内源性衰老，还会经历外源性衰老。虽然外源性皮肤衰老已得到广泛研究，但内源性皮肤衰老的发病机制仍远未明确。内源性皮肤衰老反映了在内部器官中常见的衰退过程。这些过程包括细胞衰老和增殖能力下降、细胞DNA修复能力降低和染色体异常、端粒丢失、核外线粒体DNA点突变、氧化应激和基因突变。因此，未暴露部位的老化皮肤表现出典型特征，包括细纹、干燥、暗沉和弹性丧失。最近的数据表明，随着年龄增长出现的激素缺乏也可能导致衰老表型。据报道，绝经后女性接受激素替代疗法或局部雌激素治疗后，表皮皮肤水分、弹性和皮肤厚度得到改善，表面脂质生成增加，皱纹深度减少，胶原纤维恢复，胶原III/I比值增加。此外，由人类SZ95皮脂腺细胞组成的内源性皮肤衰老体外模型在激素替代环境下培养表明，特定年龄和性别的激素能够通过调节其转录组来改变细胞的发育。总之，在其他因素中，激素环境在老化皮肤的形成中起着独特作用。
