Xinxiang Key Laboratory of Inflammation and Immunology, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan, China.
Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Expert Rev Clin Immunol. 2024 Jul;20(7):727-734. doi: 10.1080/1744666X.2024.2330604. Epub 2024 Mar 21.
Intestinal fibrosis is a common and serious complication of inflammatory bowel diseases (IBD) driving stricture formation in Crohn's disease patients and leading to submucosal damage in ulcerative colitis. Recent studies provided novel insights into the role of immune and nonimmune components in the pathogenesis of intestinal fibrosis. Those new findings may accelerate the development of anti-fibrotic treatment in IBD patients.
This review is designed to cover the recent progress in mechanistic research and therapeutic developments on intestinal fibrosis in IBD patients, including new cell clusters, cytokines, proteins, microbiota, creeping fat, and anti-fibrotic therapies.
Due to the previously existing major obstacle of missing consensus on stricture definitions and the absence of clinical trial endpoints, testing of drugs with an anti-fibrotic mechanism is just starting in stricturing Crohn's disease (CD). A biomarker to stratify CD patients at diagnosis without any complications into at-risk populations for future strictures would be highly desirable. Further investigations are needed to identify novel mechanisms of fibrogenesis in the intestine that are targetable and ideally gut specific.
肠纤维化是炎症性肠病（IBD）的一种常见且严重的并发症，可导致克罗恩病患者出现狭窄，并导致溃疡性结肠炎患者出现黏膜下损伤。最近的研究为免疫和非免疫成分在肠纤维化发病机制中的作用提供了新的见解。这些新发现可能会加速 IBD 患者抗纤维化治疗的发展。
本综述旨在涵盖 IBD 患者肠纤维化在机制研究和治疗进展方面的最新进展，包括新的细胞簇、细胞因子、蛋白质、微生物群、爬行脂肪和抗纤维化治疗。
由于以前在狭窄定义上缺乏共识，并且缺乏临床试验终点，因此具有抗纤维化机制的药物在狭窄性克罗恩病（CD）中的测试才刚刚开始。非常需要一种生物标志物，以便在没有任何并发症的情况下，在诊断时将 CD 患者分层为未来出现狭窄的高危人群。需要进一步研究以确定可靶向且理想的肠道特异性纤维化发生的新机制。
