Advances of exosome regulating‑FXR to repair inflammatory bowel disease (Review)

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Inflammatory bowel disease (IBD), which encompasses ulcerative colitis and Crohn's disease, poses significant treatment difficulties because of its persistent course and underlying inflammatory mechanisms. Existing treatments primarily focus on alleviating symptoms, while novel biological drugs that target specific molecular pathways could address the root causes of the disease. One such pathway involves the farnesoid X receptor (FXR), a nuclear receptor essential for bile acid metabolism, intestinal homeostasis and modulation of inflammation. Activating FXR can reduce intestinal inflammation and improve gut barrier function, highlighting its potential as a treatment target for IBD. However, using synthetic agonists to directly activate FXR has drawbacks, including off‑target effects and limited effectiveness. Exosomes, tiny nanoscale vesicles involved in cell‑to‑cell communication, have emerged as promising therapeutic tools for regulating FXR signaling in IBD. Exosomes, particularly those derived from mesenchymal stem cells, can deliver bioactive molecules that promote FXR activation, reduce inflammation, and enhance tissue regeneration. The present review examines how exosomes regulate FXR signaling and their potential therapeutic use in IBD. It covers exosome biogenesis, therapeutic benefits and their molecular mechanisms in IBD.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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