肠黏膜损伤是多种疾病发生和发展的病理生理学基础，研究烧伤应激后急性肠黏膜损伤过程的信号转导通路以及后续自我修复过程中的分子机制有重要的价值。在前期的研究中，本课题组系统性地阐明了肠三叶因子（ITF）在肠黏膜保护和修复过程中的作用以及相关分子调控机制，并提出了ITF可以激活JAK/STAT3通路并启动自身转录（即“自身诱导”作用）；在后续的研究中，我们又意外发现烧伤动物模型中肠黏膜的自噬能力增强，并且提高自噬水平有利于受损肠黏膜的进一步修复，同时发现长链非编码RNA（lncRNA）在这一过程中起到了重要的调控作用。在本研究中，我们基于前期的研究成果，提出烧伤后肠道可能通过“内质网应激-自噬-lncRNA-ITF”这一途径实现修复的假说，并且将对于这一通路中的细节进行完善。通过对于本通路的研究，我们将进一步给出未来临床中用于实现受损肠黏膜修复的基因治疗与化学小分子抑制剂治疗的实验基础。

Intestinal mucosal injury is the pathophysiologic basis of the occurrence and development of various diseases. It is of great value to explore the signal transduction pathway during traumatic stress-induced acute intestinal mucosal injury and the following self-repair process. In the previous study, we systematically clarified the role of intestinal trefoil factor (ITF) in the process of intestinal mucosal protection and repair as well as the underlying mechanism; we demonstrated that ITF can activate JAK/STAT3 signaling pathway and initiate ITF transcription. Subsequently, we found that the autophagy of the intestinal mucosa in the burned animal model was enhanced, which was favorable for repair of intestinal mucosa; moreover, we found that long non-coding RNA (lncRNA) played an important role in this process. Based on these results, this program hypothesized that the repair process of the injured intestinal tract is mediated by the "endoplasmic reticulum stress- autophagy-lncRNA-ITF" axis. This project will further provide the experimental basis for treatment of severe gastrointestinal mucosal injury using gene therapy and small-molecule inhibitors.