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The Multiple Faces of Integrin-ECM Interactions in Inflammatory Bowel Disease. | LitMetric

AI Article Synopsis

  • Inflammatory Bowel Disease (IBD) includes chronic intestinal conditions like Crohn's disease and ulcerative colitis, with fibrosis being a key feature that leads to intestinal narrowing.
  • Fibrosis in IBD often persists despite anti-inflammatory treatments, suggesting it may arise independently of inflammation.
  • Recent therapies targeting integrins show promise by influencing immune cell behavior and may provide insights into fibrotic mechanisms that don’t rely solely on inflammation.

Article Abstract

Inflammatory Bowel Disease (IBD) comprises a series of chronic and relapsing intestinal diseases, with Crohn's disease and ulcerative colitis being the most common. The abundant and uncontrolled deposition of extracellular matrix, namely fibrosis, is one of the major hallmarks of IBD and is responsible for the progressive narrowing and closure of the intestine, defined as stenosis. Although fibrosis is usually considered the product of chronic inflammation, the substantial failure of anti-inflammatory therapies to target and reduce fibrosis in IBD suggests that fibrosis might be sustained in an inflammation-independent manner. Pharmacological therapies targeting integrins have recently shown great promise in the treatment of IBD. The efficacy of these therapies mainly relies on their capacity to target the integrin-mediated recruitment and functionality of the immune cells at the damage site. However, by nature, integrins also act as mechanosensitive molecules involved in the intracellular transduction of signals and modifications originating from the extracellular matrix. Therefore, understanding integrin signaling in the context of IBD may offer important insights into mechanisms of matrix remodeling, which are uncoupled from inflammation and could underlie the onset and persistency of intestinal fibrosis. In this review, we present the currently available knowledge on the role of integrins in the etiopathogenesis of IBD, highlighting their role in the context of immune-dependent and independent mechanisms.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8508809PMC
http://dx.doi.org/10.3390/ijms221910439DOI Listing

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