Dermatology
GLP-1 Receptor Agonists Emerge as Potential Modulators of Inflammation and Angiogenesis in Wound Healing
Oct 21, 2025
AT A GLANCE
A new review explores how GLP-1 receptor agonists—best known for glycemic control—may also promote diabetic wound healing by dampening inflammation, enhancing angiogenesis, and activating cellular pathways that restore tissue repair.
Chronic diabetic foot ulcers (DFUs) remain one of the most challenging complications of diabetes, largely due to persistent inflammation, impaired angiogenesis, and delayed tissue regeneration. This new review synthesizes preclinical and mechanistic evidence showing that glucagon-like peptide-1 receptor agonists (GLP-1 RAs), a class of drugs originally developed for glucose regulation, exert significant immunomodulatory and pro-regenerative effects in the skin. Studies in vitro and in animal models demonstrate that GLP-1 RAs suppress key inflammatory mediators such as TNF-α and NF-κB while activating cellular repair pathways including AMPK and PI3K/Akt. These effects collectively enhance keratinocyte migration, improve endothelial progenitor cell function, and polarize macrophages toward wound-healing phenotypes.
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Beyond immunologic modulation, GLP-1 RAs appear to restore neutrophil antimicrobial function, optimize matrix remodeling, and stimulate angiogenic mediators like VEGFR-2 and HIF-1α, contributing to tissue perfusion and granulation. Although human trials are still lacking, these findings position GLP-1 RAs as compelling candidates for adjunctive DFU therapy, with future potential for topical or localized delivery formulations. If clinical validation follows, these agents could transform chronic wound management by targeting the metabolic-immune-vascular interface that defines diabetic tissue injury.
Reference: Ghebrehiwet-Kuflom J, Mehta A, Lim P, Dahle S, Isseroff RR. GLP-1 Receptor Agonists as Emerging Modulators of Inflammation and Angiogenesis in Chronic Cutaneous Wound Healing. J Invest Dermatol. 2025 Oct 13:S0022-202X(25)02434-0. doi: 10.1016/j.jid.2025.08.045. Epub ahead of print. PMID: 41081666.