1. Novel mechanisms and clinical trial endpoints in intestinal fibrosis
- Author
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David R. Van Wagoner, Florian Rieder, Claudio Fiocchi, Jonathan Mark Brown, Sinan Lin, and Jie Wang
- Subjects
0301 basic medicine ,medicine.medical_treatment ,Immunology ,Disease ,Constriction, Pathologic ,Biology ,Bioinformatics ,Inflammatory bowel disease ,Article ,Pathogenesis ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Crohn Disease ,Fibrosis ,medicine ,Immunology and Allergy ,Humans ,medicine.disease ,Inflammatory Bowel Diseases ,Clinical trial ,Bowel obstruction ,Intestines ,030104 developmental biology ,Cytokine ,030215 immunology - Abstract
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.
- Published
- 2021