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Transmural intestinal fibrosis involving the mesenteric fat is a prominent feature of Crohn’s disease (CD) eliciting painful complications such as stenosis and fistulas of the intestine which are well-known since the pathological and clinical entity of CD was characterised by Burrill Bernard Crohn.1
However, although the armamentarium of inflammatory bowel disease (IBD) therapies has substantially expanded—for example, by the introduction of antibodies and small molecules targeting immune cells and inflammatory pathways—there are still no anti-fibrotic medical therapeutics available in clinical practice of patient with IBD care. In fact, key elements of transmural intestinal fibrosis directed therapy are still limited to endoscopic balloon dilatation or surgical resection. Although the major clinical need is evident, some issues make studies addressing transmural intestinal fibrosis particularly difficult, for example, tissue analysis for cellular and molecular characterisations usually needs prior surgery. Moreover, clinical studies of intestinal fibrosis have remained challenging, for example, because the symptoms and individual disease burden associated with fibrosis can be highly variable, and methods to monitor reliably the degree of fibrosis in serial analyses are still restricted. Recent efforts to define standardised treatment targets and to establish a consented histopathological scoring system are important steps which could aid more successful clinical trials and drug development within this field of exceptional relevance.2 3 In addition to the challenges of fibrosis research in humans, preclinical studies are confined by the limitations of the model systems at hand. There are several in vivo systems currently available such as sporadic, chemically-induced or microbial-based models of intestinal fibrosis which all have specific pros and cons related to the triggers of fibrosis induction. However, a major constraint of all of the …
Contributors CN wrote the commentary.
Funding Funding was provided by the DFG (TRR241-A08, SFB1181-C02, NE1927/2-2, FOR2438).
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.