摘要紫外线照射可使皮肤损伤,导致皮肤光老化或皮肤肿瘤.多个信号通路如Nrf2-Keap1-ARE、核因子κB、丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇-3激酶-丝氨酸/苏氨酸激酶-西罗莫司靶蛋白(PI3K-AKt-mTOR)信号通路等参与皮肤光老化和(或)皮肤肿瘤的发病.Nrf2信号通路在氧化应激状态下开启,有维持氧化还原平衡和参与细胞新陈代谢等作用.核因子κB信号通路的激活引起基质金属蛋白酶等水平上调,与皮肤老化和非黑素性皮肤癌有关.MAPK信号通路参与皮肤老化和皮肤肿瘤的进展.PI3K-AKt-mTOR信号通路主要与皮肤肿瘤相关.紫外线照射可诱导上述通路的活化,参与皮肤光老化或皮肤肿瘤的发生发展.对上述通路的进一步研究有望为抵御皮肤的光老化和皮肤肿瘤提供新的方法.

abstractsUltraviolet radiation can cause skin damage,leading to skin photoaging and skin neoplasms.Multiple signaling pathways participate in the occurrence of skin photoaging and (or) skin neoplasms,such as Nrf2-Keap 1-ARE signaling pathway,nuclear factor-κB (NF-κB) signaling pathway,mitogen-activated protein kinase (MAPK) signaling pathway and phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K-Akt-mTOR) signaling pathway.Nrf2 signaling pathway,which is usually activated under oxidative stress,plays an important role in maintaining redox balance and participates in cell metabolism.The activation of NF-κB signaling pathway can up-regulate the level of matrix metalloproteinase (MMP),which is related to skin aging and non-melanoma skin cancers.MAPK signaling pathway participates in the development of skin aging and skin neoplasms.PI3K-Akt-mTOR signaling pathway is mainly related to skin neoplasms.Ultraviolet radiation can induce activation of the above signaling pathways,participate in the occurrence and development of skin aging and skin neoplasms.Further researches on the above signaling pathways may provide new methods for the prevention of and protection from skin photoaging or skin neoplasms.