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Photoaging is the superposition of chronic solar ultraviolet ��UV�� irradiation-induced damage and accounts for most age-associated changes in skin appearance. The molecular mechanisms of photoaging are triggered by reactive oxygen species ��ROS�� produced by skin cells after UV irradiation, which subsequently activate cell surface receptors, initiate intracellular signalling cascades, stimulate transcription factor activator proteins and nuclear factor-kappa B, and finally induce the degradation of skin extracellular matrix ��ECM�� and initiation of inflammation. Estrogen induces collagen synthesis, increases skin water content and improves the appearance and functions of photoaged skin by interfering with the transforming growth factor ��TGF-β/Smad signaling pathway, and finally prevents photoaging etiologically. Different tissues express different estrogen receptors ��ER��, and skin mainly expresses ER-β. When binding with the ligand, ER-β does not carry the breast and uterine proliferation liabilities of ER-α��therefore, to develop and utilize selective estrogen receptor activators may be of great value to the prevention and control of photoaging.

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