Division of Gastroenterology and Hepatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Center for Human Immunobiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Division of Gastroenterology and Hepatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Center for Human Immunobiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Cell Mol Gastroenterol Hepatol. 2024;17(5):703-711. doi: 10.1016/j.jcmgh.2024.01.007. Epub 2024 Jan 19.
Intestinal inflammatory fibrosis is a severe consequence of inflammatory bowel diseases (IBDs). There is currently no cure for the treatment of intestinal fibrosis in IBD. Although inflammation is necessary for triggering fibrosis, the anti-inflammatory agents used to treat IBD are ineffective in preventing the progression of intestinal fibrosis and stricture formation once initiated, suggesting that inflammatory signals are not the sole drivers of fibrosis progression once it is established. Among multiple mechanisms involved in the initiation and progression of intestinal fibrosis in IBD, stromal cells play critical roles in mediating the process. In this review, we summarize recent progress on how stromal cells regulate intestinal fibrosis in IBD and how they are regulated by focusing on immune regulation and gut microbiota. We also outline the challenges moving forward in the field.
肠道炎症性纤维化是炎症性肠病(IBD)的严重后果。目前,IBD 患者的肠道纤维化治疗尚无根治方法。尽管炎症是触发纤维化的必要条件,但用于治疗 IBD 的抗炎药物在启动后对预防肠道纤维化和狭窄形成无效,这表明一旦纤维化形成,炎症信号并不是纤维化进展的唯一驱动因素。在 IBD 中肠道纤维化的起始和进展所涉及的多种机制中,基质细胞在介导这一过程中起着关键作用。在这篇综述中,我们总结了基质细胞如何通过关注免疫调节和肠道微生物群来调节 IBD 中的肠道纤维化,以及它们是如何被调节的。我们还概述了该领域未来的挑战。
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