Overview highlights FGFs' involvement in IBD pathogenesis and their potential as therapeutic targets.
Fibroblast growth factor (FGF) constitutes a diverse family of signaling proteins involved in cell proliferation, differentiation, angiogenesis, lymphangiogenesis and tissue regeneration. Emerging evidence suggests that FGFs may also play a pivotal role in inflammatory bowel diseases (IBD). IBD, comprising Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic, relapsing inflammation of the intestines, manifested primarily by persistent abdominal pain and severe diarrhea. In IBD, by activating specific fibroblast growth factor receptors (FGFRs), FGFs modulate the immune response, promote mucosal healing, and regulate extracellular matrix (ECM) remodeling, thereby maintaining intestinal barrier integrity. Expression levels of several FGFs, including FGF1, FGF2, FGF7, and FGF10 are upregulated in IBD. These alterations often reflect disease exacerbation and correlate with inflammatory markers, suggesting the potential of FGFs as biomarkers. Furthermore, studies in animal models of various gastrointestinal (GI) tract diseases demonstrate promising possibilities for the use of recombinant FGFs as a novel therapeutic approach to managing gut inflammation.
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Jarzabek et al. (2026) studied this question.
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