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Review
. 2025 Mar;18(3):42-50.

A Review of Glucagon-like Peptide-1 in Dermatology

Willmar Patino  1 , Amanda Thomas  2 , Sanjana Jain  3 , James Q Del Rosso  4 , Naiem T Issa  5
Affiliations
Review

A Review of Glucagon-like Peptide-1 in Dermatology

Willmar Patino et al. J Clin Aesthet Dermatol. 2025 Mar.

Abstract

Objective: Glucagon-like peptide-1 (GLP-1) is a hormone produced in response to meal intake by endocrine intestinal cells. GLP-1 binds to its receptors which are expressed on various cells throughout the body. GLP-1 receptors (GLP-1R) have become a target for the treatment of diabetes mellitus and weight loss, and GLP-1 receptor agonist (GLP-1RA) use has become more common among patients. In addition to the anti-hyperglycemic effects, recent studies have exhibited anti-inflammatory effects of GLP-1RAs. Current research surrounding GLP-1Rs and GLP-1R agonism in dermatology is limited. This review aims to describe the current knowledge of GLP-1Rs and GLP-1RA use in dermatology and suggest future directions.

Methods: A literature search focused on GLP-1RAs and their effect on cutaneous disease processes was performed across various databases. The databases were searched through May 2024.

Results: The use of GLP-1RAs have shown promising anti-inflammatory effects and improvement in wound healing, psoriasis, and hidradenitis suppurativa. Several cutaneous adverse reactions to GLP-1RAs were also identified with injection site pruritus, erythema, and rash being the most commonly reported.

Limitations: Current literature is limited to case reports and small-scale studies.

Conclusion: The literature suggests anti-inflammatory effects of GLP-1RAs may provide direct benefit in the treatment of dermatologic conditions independent of glucose control in addition to indirect improvement via modulation of blood glucose and weight loss. Further studies investigating the implications of GLP-1RA use and the possible therapeutic potential of GLP-1RAs in inflammatory skin conditions are warranted.

Keywords: GLP-1 receptor agonists; cutaneous adverse effects; hidradenitis suppurativa; psoriasis; wound healing.

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Conflict of interest statement

DISCLOSURES: Dr. Issa has served as a consultant and advisor for Eli Lilly and Company. Dr. Del Rosso has served as an investigator, consultant, advisor, and/or speaker for Galderma, Abbvie, Aclaris, Almirall, Amgen, Anaptys Bio, Arcutis, Athenex, Bausch, Biofrontera, Biopharmx, Biorasi, Blue Creek, Botanix, Brickell, Bristol Meyers Squibb, Cara Therapeutics, Cassiopea, Dermata, Dermavant, Encore, Epi Health, Evommune, Ferndale, Genentech, Incyte, JEM Health, Leo Pharma, La Roche Posay, Lilly, MC2, Novan, Pfizer, Ralexar, Regeneron, Sanofi-Genzyme, Sente, SolGel, Sonoma, Sun Pharma, Trevi, UCB, Verrica, and Vyne.

Figures

FIGURE 1.
FIGURE 1.
Cutaneous expression of GLP1-Rs has been found to be clustered around hair follicles, in keratinocytes, and in infiltrating immune cells
FIGURE 2.
FIGURE 2.
There are multiple mechanisms by which GLP-1RAs are suggested to improve wound healing. These mechanisms include the anti-inflammatory and pro-healing effects of decreasing CRP and MMP-9/TIMP-1 ratio, endothelial protection and angiogenesis secondary to increased AMPK, increased endothelial cell proliferation due to stimulation of CD31+ cells, P13/AKT induced keratinocyte migration, increased vascularity and dermal and epidermal regeneration due to increased phosphorylated eNOS and VEGF R2, as well as increased endothelial progenitor cells, fibroblasts, and myofibroblasts.
FIGURE 3.
FIGURE 3.
Multiple mechanisms have been suggested to explain GLP-1RA-associated improvement in psoriasis. Studies have suggested possible mechanisms include increased iNKT cell modulation, AMPK phosphorylation, IL-23/Th17 regulation and decreased macrophage migration, phospho-IKKa/B 176/S180, phospho-JAK2, phospho-NF-kB p65, phospho-STAT3, SOCS3, TNF-a, 11-6, IL-23, IL-17, IL-22, and уб T cells.
See this image and copyright information in PMC

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