Deadline for manuscript submissions: 30 March 2026.
Fibrosis, characterised by the excessive deposition of extracellular matrix via activated fibroblasts, is a pathological feature of several chronic inflammatory disorders, which collectively contribute significantly to global morbidity and mortality. Despite this, current anti-fibrotic therapies are of limited efficacy. However, incretin-based therapies, primarily glucagon-like peptide-1 (GLP-1) receptor agonists, are now emerging as candidate drugs for modulating fibrotic signalling pathways. This review synthesises the growing body of preclinical and clinical evidence that incretin receptor agonists exert direct and indirect anti-fibrotic effects. We detail the molecular mechanisms and survey the promising data across hepatic, cardiac, renal, lung, and joint tissues, which underscore the potential for repurposing of this drug class as a therapeutic strategy for fibro-inflammatory conditions.