The miR-2110/TRAF3 axis is associated with endothelial dysfunction and atherosclerosis in coronary heart disease

Coronary heart disease (CHD) is driven by endothelial dysfunction and chronic vascular inflammation. hsa-miR-2110 (miR-2110) has been associated with adverse cardiovascular outcomes, but its mechanistic role in CHD remains unclear. In this study, miR-2110 expression was quantified in peripheral blood from CHD patients and healthy controls. Functional effects were assessed in EA.hy926 endothelial cells following lentiviral overexpression of miR-2110. The target gene TRAF3 was identified by RNA sequencing, bioinformatic analysis, and validated by dual-luciferase reporter assays, RT-qPCR, and Western blotting. TRAF3 expression was further evaluated in CHD patient blood samples and in atherosclerotic lesions from ApoE^-/- mice fed a high-fat diet. miR-2110 was significantly downregulated in CHD patients. Overexpression of miR-2110 in endothelial cells impaired proliferation and migration, induced S-phase arrest, reduced apoptosis, and promoted cellular senescence. TRAF3 was confirmed as a direct target of miR-2110. TRAF3 was significantly upregulated in CHD patients. In ApoE^-/- mice, TRAF3 protein expression was increased in atherosclerotic lesions, predominantly within the tunica intima. Pathway enrichment predicted NF-κB-related signaling among the enriched pathways potentially associated with the miR-2110/TRAF3 axis. Together, our findings suggest that the miR-2110/TRAF3 axis represents a novel regulatory pathway involved in CHD, potentially relevant to endothelial dysfunction and inflammatory signaling.