Journal
CLINICAL SCIENCE
Volume 129, Issue 12, Pages 1107-1113Publisher
PORTLAND PRESS LTD
DOI: 10.1042/CS20150472
Keywords
Crohn's disease; collagen; extracellular matrix; Smad; TGF-beta 1
Categories
Funding
- Giuliani SpA
- Broad Medical Research Foundation
- Novo Nordisk
- Teva
- Sirtris
- Lycera
- Sofar
- AbbVie
- Zambon
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In Crohn's disease, one of the two major forms of inflammatory bowel diseases in human beings, persistent and chronic inflammation promotes fibrotic processes thereby facilitating formation of strictures, the most common indication for surgical intervention in this disorder. The pathogenesis of Crohn's disease-associated fibrosis is not fully understood, but variants of genes involved in the recognition of microbial components/products [e.g. CARD15 (caspase-activating recruitment domain 15) and ATG16L1 (autophagy-related 16-like 1)] are associated with this phenotype, and experimental evidence suggests that intestinal fibrosis results from an altered balance between deposition of ECM (extracellular matrix) and degradation of ECM by proteases. Studies have also contributed to identify the main phenotypic and functional alterations of cells involved in the fibrogenic process, as well as molecules that stimulate such cells to produce elevated amounts of collagen and other ECM-related proteins. In the present review, we assess the current knowledge about cellular and molecular mediators of intestinal fibrosis and describe results of recent studies aimed at testing the preventive/therapeutic effect of compounds in experimental models of intestinal fibrosis.
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