过量紫外线B（UVB）照射是导致多种严重皮肤疾病的关键因素，研究显示circRNA可能在其中扮演着重要的角色，但其具体过程和机制并不清楚。我们前期研究发现：circFBXW8是影响皮肤上皮细胞UVB照后细胞功能改变的关键circRNA；eIF4A3、miR-664可能分别作为circFBXW8的上游和下游信号分子参与到UVB辐射损伤应激调控中。在此基础上，本项目以HaCaT细胞、Balb/c小鼠及circFBXW8敲入小鼠的急/慢性UVB辐射损伤皮肤组织为观察对象，研究circFBXW8在急/慢性UVB辐射损伤应激进程中作用，探索eIF4A3，miR-664参与该调控进程的分子机制，从而明确UVB辐射损伤应激中的eIF4A3-circFBXW8-miR-664调控轴。该研究结果将有助于深化对UVB辐射损伤应激调控机制的认识，并可为其损伤防治提供新的靶点。

Excessive ultraviolet B (UVB) exposure is one of the crucial factors for a variety of severe skin diseases. Studies have shown that circRNA may play an important role in these diseases, but the specific process and mechanism are unclear. Our previous study have confirmed that: circFBXW8 is the key circRNA affecting the function of UVB irradiated skin epithelial cells ; eIF4A3 and miR-664 may be respectively involved in the regulation of UVB radiation response as the upstream or downstream molecule of circFBXW8. Based on these data, HaCaT cell, Balb/c mice and circFBXW8 knock-in mice in acute and chronic radiation models will be employed to study the role of circFBXW8 in UVB radiation stress injury with the evaluation of irradiated skin lesions. Next, we will explore the molecular mechanism of which eIF4A3 and miR-664 are involved in this regulatory process, and establish eIF4a3-circFBXW8-miR-664 regulatory axis in UVB radiation damage response. This research will deepen the understanding of UVB radiation damage stress mechanism and find a novel target for UVB radiation damage prevention and treatment.