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Antiinflammatory actions of glucagon-like peptide-1–based therapies beyond metabolic benefits
Chi Kin Wong, Daniel J. Drucker
Chi Kin Wong, Daniel J. Drucker
Published November 3, 2025
Citation Information: J Clin Invest. 2025;135(21):e194751. https://doi.org/10.1172/JCI194751.
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Review Series

Antiinflammatory actions of glucagon-like peptide-1–based therapies beyond metabolic benefits

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Abstract

Therapies based on glucagon-like peptide-1 (GLP-1) reduce rates of cardiovascular and chronic kidney disease in people with type 2 diabetes and/or obesity, with ongoing clinical trials investigating their effects in people with metabolic liver disease, arthritis, and both substance use and neurodegenerative disorders. Acute and chronic activation of GLP-1 receptor signaling also reduces systemic and tissue inflammation in mice and humans, through weight loss–dependent and –independent mechanisms, actions that may contribute to the expanding spectrum of clinical benefits ascribed to GLP-1 medicines. In this Review, we highlight current understanding of the direct and indirect antiinflammatory effects and mechanisms of GLP-1 medicines in both preclinical and clinical studies, covering emerging concepts, clinical relevance, and areas of uncertainty that require further investigation.

Authors

Chi Kin Wong, Daniel J. Drucker

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Figure 1

Antiinflammatory actions of GLP-1 medicines across organs.

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Antiinflammatory actions of GLP-1 medicines across organs.
GLP-1R agonis...
GLP-1R agonists exert broad antiinflammatory effects in multiple peripheral organs, including the central nervous system, lungs, cardiovascular system, liver, intestine, kidneys, and joints. Evidence from both preclinical and clinical studies supports their antiinflammatory roles in the cardiovascular system, liver, kidneys, and joints. However, the potential antiinflammatory effects of GLP-1 signaling in the central nervous system, lungs, and intestine remain to be fully elucidated and warrant further investigation.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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