Abstract
Intestinal fibrosis, driven by chronic inflammation in Crohn's disease, can be defined as an excessive accumulation of extracellular matrix in the affected gut segment ultimately leading to an impaired wound healing and cumulative tissue damage, possibly resulting in organ dysfunction, formation of stenotic lesions and necessity of surgical intervention. Despite continuous advances in developing novel treatment modalities targeting different pathways to control chronic gut inflammation in CD, no effective anti-fibrotic agents have been released, to date. Thus, a better understanding of the molecular and cellular mechanisms underlying intestinal fibrosis is key to move this area of investigation forward.
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