Synergistic SGLT2 and GLP-1R targeting alleviates systemic inflammation-induced and M1 monocyte-driven endothelial dysfunction in coronary artery disease.

Date publication

juillet 2026

Journal

Cardiovascular diabetology

Auteurs

Membres identifiés du Cancéropôle Est :
Pr SCHINI-KERTH Valérie

Tous les auteurs :
Mroueh A, Fakih W, Kerth S, Kikuchi S, Aboueddahab C, Gong DS, Choi M, Nicolas A, Fass S, Trimaille A, Granier A, Carmona A, Amissi S, Pompach P, Oak MH, Jesel L, Görlach A, Morel O, Schini-Kerth V

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/42401896

Résumé

Systemic residual inflammation plays a pivotal role in the pathophysiology of coronary artery disease (CAD). Cardiovascular protection by SGLT2 inhibitors (SGLT2i) and GLP-1 receptor agonists (GLP-1Ra) is associated with reduced inflammatory burden but underlying cellular mechanisms remain incompletely defined. We investigated whether SGLT2i and GLP-1Ra synergistically suppress monocyte activation and prevent both systemic inflammatory mediator-induced and monocyte-driven endothelial dysfunction in CAD.

Mots clés

Coronary artery disease, GLP-1R agonists, Inflammation, Monocyte-endothelial crosstalk, SGLT2 inhibitors

Référence

Cardiovasc Diabetol. 2026 07 4;: