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Preclinical studies have elucidated multiple direct anti-atherogenic mechanisms of GLP-1 RAs, including suppression of pro-inflammatory cytokine production (TNF-α, IL-1β, IL-6) in macrophages, inhibition of monocyte adhesion to endothelial cells through downregulation of adhesion molecules, reduction of oxidized LDL-induced foam cell formation, and attenuation of atherosclerotic plaque development in murine models (72–74)
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