KLF5 (Krüppel-like factor 5)是在肠隐窝底部增殖细胞中高表达的锌指蛋白转录因子，对于维持肠道隐窝结构和屏障功能起重要作用。前期研究工作表明电离辐射诱导小鼠小肠组织KLF5的表达与病情的进展具有相关性，提示KLF5可能具有参与修复放射性肠损伤的作用。鉴于此，本项目拟在分子、细胞和动物整体不同水平上，分析不同剂量照射对正常小肠上皮细胞表达KLF5的影响及其上游调控机制，明确KLF5是否参与放射性肠损伤修复并探索其参与修复的途径，从而揭示KLF5在放射性肠损伤中的作用机制，为阐明急性肠型辐射损伤机制以及寻找新的救治途径提供理论依据。

KLF5 (Krüppel-like factor 5) is a zinc finger-containing transcription factor, which is expressed in proliferating epithelial cells at the base of the intestinal crypts. KLF5 plays a very important role in maintaining crypt architecture and barrier function. Preliminary results showed that intestinal KLF5 protein in mice was induced upon ionizing radiation (IR). Dynamic expression of KLF5 was associated with progression of disease, suggesting that KLF5 may be crucial in repairing intestinal radiation injury. Therefore, this project will further investigate the molecular mechanisms of how KLF5 is induced by IR and the involvement of KLF5 in repairing intestinal radiation injury on molecular, cellular and animal levels. The understanding of the role and mechanism of KLF5 in radiation-induced intestinal damage will help establish the theoretical foundation for gaining insights into the pathogenesis underlying acute gastrointestinal syndrnme and developing novel therapeutic approaches.