光老化
光化性角化病
皮肤病科
医学
皮肤老化
色素沉着
紫外线
光防护
紫外线辐射
DNA损伤
病理
光性皮炎
皮肤癌
化学
色素性干皮病
DNA
基底细胞
光合作用
放射化学
光化学
生物化学
作者
Cemal Bilaç,Mustafa Turhan Şahin,Serap Öztürkcan
标识
DOI:10.1016/j.clindermatol.2014.02.014
摘要
Chronic actinic damage of the skin manifests itself as extrinsic skin aging (photoaging) and photocarcinogenesis. During the last decade, substantial progress has been made in understanding cellular and molecular mechanisms of photoaging. DNA photodamage and ultraviolet-generated reactive oxygen species are the initial events that lead to most of the typical histologic and clinical manifestations of chronic photodamage of the skin. Chronic actinic damage affects all layers of the skin. Keratinocytes, melanocytes, fibroblasts, and endothelial cells are altered by ultraviolet radiation and can result in numerous changes in human skin, particularly the skin of fair-skinned individuals. These changes include actinic keratosis, thickening and wrinkling, elastosis, telengiectasia, solar comedones, diffuse or mottled hyperpigmentation, and skin cancers. There are many options in the treatment of changes caused by chronic actinic damage. The most effective measure of prevention of the photoaging and photocarcinogenesis is sun protection.
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