临床中有许多炎症性、肿瘤性皮肤病与光损伤相关，明确光损伤的发病机制，对预防和治疗此类皮肤病具有重要的临床意义。前期课题组通过比较人体不同年龄段、曝光与非曝光部位皮肤组织寻找到差异蛋白：热休克蛋白27；并在细胞水平和动物模型中证明在皮肤光损伤中HSP27通过抗凋亡起到保护作用；同时国内外研究发现，细胞自噬也可能通过调控凋亡参与到光损伤皮肤病的发病过程中。但HSP27与自噬之间是否存在关联、是否共同调控细胞的存活尚需进一步研究。本项目以皮肤成纤维细胞为研究对象，用UVB诱导急、慢性光损伤模型，阐明HSP27及自噬在光损伤中的作用，通过干预HSP27探究其是否通过P53/AMPK、PI3K-AKT-mTOR途径诱导或是抑制自噬，旨在揭示HSP27与自噬在光损伤中共同影响细胞凋亡、存活，从而发挥保护作用的可能机制。为探究UV相关皮肤病及肿瘤的内在联系提供新思路，为防治此类皮肤病奠定理论基础。

There are many inflammatory and neoplastic skin diseases associated with photodamage in clinic.The pathogenesis of photodamage is of great importance for the prevention and treatment of such skin diseases. The study group has found the differential protein: heat shock protein 27 by comparing the human skin tissue between exposed and non-exposed parts at different ages; we have proved that HSP27 plays a protective role in skin photodamage through anti-apoptosis at the cellular and animal models.Some research groups also found that autophagy might be involved in the pathogenesis of UV-induced photodamaged skin diseases. However, whether there is an association between HSP27 and autophagy and they co-regulate cell survival are still needed to be solved in further study. In this project, human skin fibroblasts (HSF) will be used as the research object, and UVB will be used to induce acute and chronic photodamage models. We are going to elucidate the protective effects of HSP27 and autophagy in photodamage, and to determine whether HSP27 play an anti-apoptotic effect through regulating autophagy by PI3K-AKT-mTOR pathway and P53/AMPK pathway. This research will study the possible molecular mechanism of HSP27 and autophagy in dermatitis caused by photodamage, in order to provide new ideas for investigating the intrinsic link between UV-related skin diseases and tumors, and also lay a theoretical foundation for the prevention and treatment of such skin diseases.