Molecular Basis of Intestinal Fibrosis in Inflammatory Bowel Disease.

Q2 Medicine Inflammatory Intestinal Diseases Pub Date : 2023-03-01 DOI:10.1159/000528312
Akira Andoh, Atsushi Nishida
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引用次数: 3

Abstract

Background: Intestinal fibrosis in Crohn's disease (CD) is considered to be irreversible and induces persistent luminal narrowing and strictures. In the past decades, substantial advances have been made in the understanding of the cellular and molecular mechanisms underlying intestinal fibrosis in inflammatory bowel disease (IBD).

Summary: Intestinal fibrosis is typically associated with mesenchymal cell hyperplasia, tissue disorganization, and deposition of extracellular matrix (ECM). The transient appearance of mesenchymal cells is a feature of normal wound healing, but the persistence of these cells is associated with ECM deposition and fibrosis, leading to loss of normal architecture and function. When homeostatic control of the repair process becomes dysregulated, perpetual activation of profibrotic responses and sustained accumulation of ECM are induced. In the process of intestinal fibrosis, myofibroblasts are considered to be the key effector cells, being responsible for the synthesis of ECM proteins. Activation and accumulation of myofibroblasts in the stricturing lesions of CD patients are mediated by various factors such as growth factors, cytokines, epithelial-to-mesenchymal or endothelial-to-mesenchymal transitions. Despite the identification of many putative targets and target pathways applicable to antifibrotic therapies, no such treatment has yet been successful. Predictive biomarkers and non-invasive diagnostic tools for intestinal fibrosis are still insufficient in IBD.

Key message: We summarize recent advances in the understanding of the cellular and molecular mechanisms underlying intestinal fibrosis in IBD.

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炎症性肠病肠纤维化的分子基础。
背景:肠纤维化在克罗恩病(CD)被认为是不可逆的,并诱导持续的管腔狭窄和狭窄。在过去的几十年里,在理解炎症性肠病(IBD)肠道纤维化的细胞和分子机制方面取得了实质性进展。摘要:肠纤维化通常与间充质细胞增生、组织紊乱和细胞外基质(ECM)沉积有关。间充质细胞的短暂出现是正常伤口愈合的一个特征,但这些细胞的持续存在与ECM沉积和纤维化有关,导致正常结构和功能的丧失。当修复过程的稳态控制失调时,促纤维化反应的永久激活和ECM的持续积累就会被诱导。在肠纤维化过程中,肌成纤维细胞被认为是关键的效应细胞,负责ECM蛋白的合成。肌成纤维细胞在CD患者狭窄病变中的激活和积累是由多种因素介导的,如生长因子、细胞因子、上皮到间质或内皮到间质转化。尽管确定了许多适用于抗纤维化治疗的假定靶点和靶点通路,但尚未有此类治疗成功。在IBD中,预测肠纤维化的生物标志物和非侵入性诊断工具仍然不足。关键信息:我们总结了IBD肠道纤维化的细胞和分子机制的最新进展。
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来源期刊
Inflammatory Intestinal Diseases
Inflammatory Intestinal Diseases Medicine-Gastroenterology
CiteScore
4.50
自引率
0.00%
发文量
6
审稿时长
20 weeks
期刊最新文献
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