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Tagami et al., 2014)
Preclinical and clinical studies have demonstrated that GLP-1 receptors expressed in myocardial and vascular endothelium tissue play a fundamental role in the cardioprotective effect of GLP-1 RAs, lowering the risk of major cardiovascular events, heart failure, and kidney complications in adults with and without diabetes [4]
The anti-inflammatory pathways modulated by GLP-1 receptor activation (NF-kB suppression, macrophage polarization, Treg enhancement) are largely distinct from the pathways targeted by: Methotrexate: Folate metabolism disruption, different anti-inflammatory pathway TNF inhibitors (adalimumab, etanercept): Direct TNF blockade, whereas GLP-1 reduces TNF production upstream IL-6 inhibitors (tocilizumab): Receptor-level blockade, while GLP-1 reduces IL-6 production JAK inhibitors (tofacitinib, baricitinib): Different signaling pathway entirely Corticosteroids: Broad immunosuppression, while GLP-1 is immunomodulatory This pathway complementarity is why additive benefit is biologically plausible
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