皮肤光老化的出现不仅严重影响皮肤美观，还与皮肤肿瘤的发生密切相关。目前光老化的发生机制尚未完全阐明，并缺乏特异性防治方法。我们的前期研究发现：UVB可导致细胞内多种miRNA表达异常，但机制不明；lincRNA RP11-255G12.2和衰老相关基因KRT16在光老化皮肤中表达减少，且二者均存在可与miR-4471结合的互补序列。因此我们推测RP11-255G12.2可能通过与miR-4471竞争性结合，从而调控KRT16的表达而参与光老化进程。为填补lncRNA在人体自然光老化皮肤组织中的作用及其机制的研究空白，本研究将应用分子生物学、生物信息学、细胞生物学研究不同年龄段人群的曝光部位和非曝光部位皮肤中RP11-255G12.2的表达差异及与临床表现的关系，探索RP11-255G12.2在光老化过程中的作用机制，为进一步阐明光老化的发生机制提供理论基础。

The appearance of skin photoaging not only affects the appearance of the skin greatly, but also closely related to the Incidence of skin tumors. At present, the mechanism of photoaging has not been fully elucidated, and there is no specific prevention and treatment based on pathophysiological processes of photoaging. Our previous study found that UVB can cause abnormal expression of many miRNAs in cells, but the mechanism is unknown; lincRNA RP11-255G12.2 and aging-related gene KRT16 are decreased in photoaging skin, and both can complementarily bind to miR-4471. Therefore, we speculate that RP11-255G12.2 may participate in the photoaging process by regulating the expression of KRT16 through competitively combined with miR-4471. In order to fill the gaps in the role and mechanism of lncRNAs in natural photoaging skin tissues, this study will apply molecular biology, bioinformatics, and cell biology to study RP11-255G12.2 in exposed and unexposed skin of people of different ages. By study the difference in expression of RP11-255G12.2 and its relationship with clinical manifestations to explore the role and mechanism of RP11-255G12.2 in photoaging process. Our findings will provide a theoretical basis for further elucidating the mechanism of photoaging.