FoxM1 is involved in the regeneration of several organs after injury and expressed in the intestinal mucosa. The intrinsic mechanism of FoxM1 activity in the mucosa after intestinal ischemia/reperfusion (I/R) injury has not been reported. Therefore, we investigated the role of FoxM1 in mediating intestinal mucosa regeneration after I/R injury. Expression of FoxM1 and the proliferation of intestinal mucosa epithelial cells were examined in rats with intestinal I/R injury and an IEC-6 cell hypoxia/reperfusion (H/R) model. The effects of FoxM1 inhibition or activation on intestinal epithelial cell proliferation were measured. FoxM1 expression was consistent with the proliferation of intestinal epithelial cells in the intestinal mucosa after I/R injury. Inhibition of FoxM1 expression led to the downregulation of Ki-67 expression mediated by the inhibited expression of Nurr1, and FoxM1 overexpression promoted IEC-6 cell proliferation after H/R injury through activating Nurr1 expression. Furthermore, FoxM1 directly promoted the transcription of Nurr1 by directly binding the promoter of Nurr1. Further investigation showed low expression levels of FoxM1, Nurr1, and Ki-67 in the intestinal epithelium of patients with intestinal ischemic injury. FoxM1 acts as a critical regulator of intestinal regeneration after I/R injury by directly promoting the transcription of Nurr1. The FoxM1/Nurr1 signaling pathway represents a promising therapeutic target for intestinal I/R injury and related clinical diseases.

FoxM1 参与损伤后多个器官的再生并在肠黏膜中表达。肠道缺血/再灌注 (I/R) 损伤后黏膜中 FoxM1 活性的内在机制尚未见报道。因此，我们研究了 FoxM1 在 I/R 损伤后介导肠黏膜再生中的作用。在肠 I/R 损伤和 IEC-6 细胞缺氧/再灌注 (H/R) 模型大鼠中检测 FoxM1 的表达和肠黏膜上皮细胞的增殖。测量了 FoxM1 抑制或激活对肠上皮细胞增殖的影响。FoxM1的表达与I/R损伤后肠黏膜上皮细胞的增殖一致。FoxM1表达的抑制导致Nurr1表达抑制介导的Ki-67表达下调，FoxM1过表达通过激活Nurr1表达促进H/R损伤后IEC-6细胞增殖。此外，FoxM1 通过直接结合 Nurr1 的启动子直接促进了 Nurr1 的转录。进一步调查显示，肠缺血性损伤患者肠上皮中 FoxM1、Nurr1 和 Ki-67 的表达水平较低。FoxM1 通过直接促进 Nurr1 的转录，作为 I/R 损伤后肠道再生的关键调节因子。FoxM1/Nurr1 信号通路代表了肠道 I/R 损伤和相关临床疾病的有希望的治疗靶点。FoxM1过表达通过激活Nurr1表达促进H/R损伤后的IEC-6细胞增殖。此外，FoxM1 通过直接结合 Nurr1 的启动子直接促进了 Nurr1 的转录。进一步调查显示，肠缺血性损伤患者肠上皮中 FoxM1、Nurr1 和 Ki-67 的表达水平较低。FoxM1 通过直接促进 Nurr1 的转录，作为 I/R 损伤后肠道再生的关键调节因子。FoxM1/Nurr1 信号通路代表了肠道 I/R 损伤和相关临床疾病的有希望的治疗靶点。FoxM1过表达通过激活Nurr1表达促进H/R损伤后的IEC-6细胞增殖。此外，FoxM1 通过直接结合 Nurr1 的启动子直接促进了 Nurr1 的转录。进一步调查显示，肠缺血性损伤患者肠上皮中 FoxM1、Nurr1 和 Ki-67 的表达水平较低。FoxM1 通过直接促进 Nurr1 的转录，作为 I/R 损伤后肠道再生的关键调节因子。FoxM1/Nurr1 信号通路代表了肠道 I/R 损伤和相关临床疾病的有希望的治疗靶点。和 Ki-67 在肠缺血性损伤患者的肠上皮中。FoxM1 通过直接促进 Nurr1 的转录，作为 I/R 损伤后肠道再生的关键调节因子。FoxM1/Nurr1 信号通路代表了肠道 I/R 损伤和相关临床疾病的有希望的治疗靶点。和 Ki-67 在肠缺血性损伤患者的肠上皮中。FoxM1 通过直接促进 Nurr1 的转录，作为 I/R 损伤后肠道再生的关键调节因子。FoxM1/Nurr1 信号通路代表了肠道 I/R 损伤和相关临床疾病的有希望的治疗靶点。