The incidence of inflammatory bowel diseases (IBD) worldwide has resulted in a global public health challenge. Intestinal fibrosis leading to stricture formation and bowel obstruction is a frequent complication in Crohn's disease (CD), and the lack of anti-fibrotic therapies makes elucidation of fibrosis mechanisms a priority. Progress has shown that mesenchymal cells, cytokines, microbial products, and mesenteric adipocytes are jointly implicated in the pathogenesis of intestinal fibrosis. This recent information puts prevention or reversal of intestinal strictures within reach through innovative therapies validated by reliable clinical trial endpoints. Here, we review the role of immune and non-immune components of the pathogenesis of intestinal fibrosis, including new cell clusters, cytokine networks, host-microbiome interactions, creeping fat, and their translation for endpoint development in anti-fibrotic clinical trials.

中文翻译：

---

肠纤维化的新机制和临床试验终点*

全球炎症性肠病 (IBD) 的发病率已导致全球公共卫生挑战。导致狭窄形成和肠梗阻的肠纤维化是克罗恩病 (CD) 的常见并发症，并且缺乏抗纤维化疗法使得阐明纤维化机制成为当务之急。进展表明，间充质细胞、细胞因子、微生物产物和肠系膜脂肪细胞共同参与了肠纤维化的发病机制。这一最新信息通过可靠的临床试验终点验证的创新疗法，使预防或逆转肠道狭窄变得触手可及。在这里，我们回顾了免疫和非免疫成分在肠纤维化发病机制中的作用，包括新的细胞簇、细胞因子网络、宿主-微生物组相互作用、