间质性膀胱炎/膀胱疼痛综合征（IC/BPS）病因复杂且难以治愈。我们研究发现，尿源干细胞（USCs）能促进IC/BPS膀胱上皮修复，然而其具体机制不明。前期工作发现：抑制外泌体分泌后，USCs的修复效果显著降低；直接应用USCs的外泌体（USCs-Exo）能降低膀胱上皮中CKAP4的表达，激活p-AKT及其下游蛋白的表达响应，促进上皮修复。小RNA测序发现USCs-Exo中含有多种microRNAs表达，其中miR-29a-3p在USCs-Exo治疗后的上皮中表达升高；生物信息学分析发现miR-29a-3p能靶向CKAP4。据此我们提出假说：USCs-Exo内miR-29a-3p调控CKAP4/AKT信号通路促进IC/BPS膀胱上皮修复。本项目拟通过干预miR-29a-3p表达，从体内、体外实验阐明USCs促进膀胱上皮修复的具体机制，为IC/BPS的临床治疗提供新的策略。

Interstitial cystitis/bladder pain syndrome (IC/BPS) is complicated and difficult to treat. Our previous study confirmed that urine-derived stem cells (USCs) could promote the bladder epithelial repair of IC/BPS, but the underlying therapeutic mechanism of USCs is unknown. In our preliminary experiment, we found that after inhibiting exosome secretion, the efficacy of USCs was significantly reduced. Direct application of exosomes from USCs (USCs-Exo) could reduce the expression of CKAP4 in bladder epithelium, activate the expression response of p-AKT and its downstream proteins, and promote epithelial repair. The expression of multiple microRNAs was confirmed in USCs-Exo through small RNA sequencing, among which miR-29a-3p was specifically up-regulated in the epithelial cells after treatment. Bioinformatics analysis revealed that miR-29a-3p could target CKAP4. Based on these, we hypothesized that exosomal miR-29a-3p from USCs promotes the bladder epithelial repair of IC/BPS through the CKAP4/AKT signaling pathway. We intends to elucidate the specific mechanism of USCs promoting bladder epithelial repair through in vivo and in vitro experiments by interfering with the expression of mir-29a-3p, so as to provide a new strategy for the clinical treatment of IC/BPS.