<h4>Objective</h4>This study aimed to investigate the mechanism by which GLP-1 RAs activate the Sema3A/NRP1 signaling pathway to alleviate inflammation and endothelial dysfunction in atherosclerosis (AS).<h4>Methods</h4>Ten 8-week-old male C57BL/6J mice served as controls (CON) and received intraperitoneal injections of saline every 2 days. The gene discussed is NRP1; the disease is endothelial dysfunction.