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重新审视炎症性肠病中的纤维化:肠道增厚。

Revisiting fibrosis in inflammatory bowel disease: the gut thickens.

作者信息

D'Alessio Silvia, Ungaro Federica, Noviello Daniele, Lovisa Sara, Peyrin-Biroulet Laurent, Danese Silvio

机构信息

PhoenixLAB, Lodi, Italy.

Department of Gastroenterology and Endoscopy, IRCCS Ospedale San Raffaele, Milan, Italy.

出版信息

Nat Rev Gastroenterol Hepatol. 2022 Mar;19(3):169-184. doi: 10.1038/s41575-021-00543-0. Epub 2021 Dec 7.


DOI:10.1038/s41575-021-00543-0
PMID:34876680
Abstract

Intestinal fibrosis, which is usually the consequence of chronic inflammation, is a common complication of inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis. In the past few years, substantial advances have been made in the areas of pathogenesis, diagnosis and management of intestinal fibrosis. Of particular interest have been inflammation-independent mechanisms behind the gut fibrotic process, genetic and environmental risk factors (such as the role of the microbiota), and the generation of new in vitro and in vivo systems to study fibrogenesis in the gut. A huge amount of work has also been done in the area of biomarkers to predict or detect intestinal fibrosis, including novel cross-sectional imaging techniques. In parallel, researchers are embarking on developing and validating clinical trial end points and protocols to test novel antifibrotic agents, although no antifibrotic therapies are currently available. This Review presents the state of the art on the most recently identified pathogenic mechanisms of this serious IBD-related complication, focusing on possible targets of antifibrotic therapies, management strategies, and factors that might predict fibrosis progression or response to treatment.

摘要

肠道纤维化通常是慢性炎症的结果,是炎症性肠病(IBD)的常见并发症,包括克罗恩病和溃疡性结肠炎。在过去几年中,肠道纤维化的发病机制、诊断和管理领域取得了重大进展。肠道纤维化过程背后与炎症无关的机制、遗传和环境风险因素(如微生物群的作用),以及用于研究肠道纤维化形成的新的体外和体内系统,都特别引人关注。在预测或检测肠道纤维化的生物标志物领域也开展了大量工作,包括新型横断面成像技术。与此同时,尽管目前尚无抗纤维化疗法,但研究人员正着手开发和验证临床试验终点及方案,以测试新型抗纤维化药物。本综述介绍了这种严重的IBD相关并发症最新确定的致病机制的现状,重点关注抗纤维化治疗的可能靶点、管理策略以及可能预测纤维化进展或治疗反应的因素。

相似文献

[1]
Revisiting fibrosis in inflammatory bowel disease: the gut thickens.

Nat Rev Gastroenterol Hepatol. 2022-3

[2]
Mechanisms of initiation and progression of intestinal fibrosis in IBD.

Scand J Gastroenterol. 2015-1

[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
Immunological Regulation of Intestinal Fibrosis in Inflammatory Bowel Disease.

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[10]
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J Pathol Transl Med. 2023-1

引用本文的文献

[1]
Pitavastatin reduces intestinal fibrosis in chronic colitis and inhibits colon fibroblast activation by enhancing MMP-9 expression via the IGF-1/IGF-1R pathway.

Braz J Med Biol Res. 2025-8-22

[2]
CRIF1 gene therapy ameliorates inflammatory bowel disease by suppressing TH17 cells and fibrosis through mitochondrial function regulation.

Front Immunol. 2025-7-31

[3]
Amphiregulin in Fibrotic Diseases and Cancer.

Int J Mol Sci. 2025-7-19

[4]
Isovaleric acid alleviates food allergy-related constipation in mice via repairing serotonin synthesis in serotonergic neurons.

Pediatr Res. 2025-7-25

[5]
Quantitative assessment of mucosal fibrosis and its correlation with disease severity and outcome in cats with chronic enteropathy.

J Feline Med Surg. 2025-7

[6]
Mineralocorticoid receptor activation contributes to intestinal fibrosis through neutrophil gelatinase-associated lipocalin in preclinical models.

Nat Commun. 2025-7-9

[7]
ER stress genes () predicts IKK-16 as a Candidate therapeutic target for colitis-related inflammation and fibrosis suppression.

Front Immunol. 2025-6-18

[8]
ECM formation and degradation during fibrosis, repair, and regeneration.

NPJ Metab Health Dis. 2025-6-10

[9]
Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses.

Sci Rep. 2025-7-2

[10]
Targeting the double-edged sword: cytokines in the pathogenesis and treatment of autoimmune diseases.

Inflammopharmacology. 2025-6-28

本文引用的文献

[1]
Novel mechanisms and clinical trial endpoints in intestinal fibrosis.

Immunol Rev. 2021-7

[2]
Adherent invasive Escherichia coli (AIEC) strain LF82, but not Candida albicans, plays a profibrogenic role in the intestine.

Gut Pathog. 2021-1-28

[3]
Incidence of and Risk Factors for Colorectal Strictures in Ulcerative Colitis: A Multicenter Study.

Clin Gastroenterol Hepatol. 2021-9

[4]
Mycobacterial Hsp65 antigen delivered by invasive Lactococcus lactis reduces intestinal inflammation and fibrosis in TNBS-induced chronic colitis model.

Sci Rep. 2020-11-18

[5]
Toll-like receptor 4 regulates intestinal fibrosis via cytokine expression and epithelial-mesenchymal transition.

Sci Rep. 2020-11-16

[6]
Betulinic acid hydroxamate prevents colonic inflammation and fibrosis in murine models of inflammatory bowel disease.

Acta Pharmacol Sin. 2021-7

[7]
AXL Is a Potential Target for the Treatment of Intestinal Fibrosis.

Inflamm Bowel Dis. 2021-2-16

[8]
Application of Human Induced Pluripotent Stem Cell-Derived Intestinal Organoids as a Model of Epithelial Damage and Fibrosis in Inflammatory Bowel Disease.

Biol Pharm Bull. 2020

[9]
Serum biomarkers of fibrostenotic Crohn's disease: Where are we now?

J Dig Dis. 2020-6

[10]
Role of non-inflammatory factors in intestinal fibrosis.

J Dig Dis. 2020-6

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