Autophagy in UV Damage Response.
Autophagy in UV Damage Response.
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DOI：
10.1111/php.12691
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发表时间：
2017-07
影响因子：
3.3
通讯作者：
He YY
中科院分区：
文献类型：
--
作者：
Sample A;He YY
来自阳光和人工晒黑床的紫外线辐射暴露是皮肤癌和皮肤光老化发展的主要风险因素。紫外线引起的皮肤损伤可以触发一系列DNA损伤反应信号通路，包括细胞周期停滞，DNA修复，以及如果损伤不可修复，细胞凋亡。代偿性增殖取代凋亡细胞以维持皮肤屏障完整性。这些过程的破坏可以通过允许受损细胞的存活和增殖来促进致癌作用。紫外线辐射还诱导自噬，这是一种分解代谢过程，可以清除不需要的或受损的蛋白质，脂质和细胞器。自噬在紫外线暴露后被激活的机制，以及自噬在紫外线响应中的功能现在才被阐明。在这里，我们总结了目前的理解，自噬调控机制的紫外线，自噬在调节细胞对紫外线诱导的光损伤的反应的作用，以及自噬调节在治疗和预防光老化和皮肤癌的影响。
UV radiation exposure from sunlight and artificial tanning beds is the major risk factor for the development of skin cancer and skin photoaging. UV-induced skin damage can trigger a cascade of DNA damage response signaling pathways, including cell cycle arrest, DNA repair, and, if damage is irreparable, apoptosis. Compensatory proliferation replaces the apoptotic cells to maintain skin barrier integrity. Disruption of these processes can be exploited to promote carcinogenesis by allowing the survival and proliferation of damaged cells. UV radiation also induces autophagy, a catabolic process that clears unwanted or damaged proteins, lipids, and organelles. The mechanisms by which autophagy is activated following UV exposure, and the functions of autophagy in UV response are only now being clarified. Here, we summarize the current understanding of the mechanisms governing autophagy regulation by UV, the roles of autophagy in regulating cellular response to UV-induced photodamage, and the implications of autophagy modulation in the treatment and prevention of photoaging and skin cancer.