MS4A6A regulates ox-LDL-induced endothelial dysfunction and monocyte adhesion in atherosclerosis via the IKK/NF-kappaB pathway

mice. In a cellular model using human umbilical vein endothelial cells (HUVECs) stimulated with oxidized low-density lipoprotein (ox-LDL), MS4A6A expression exhibited a temporal and concentration-dependent upregulation. Silencing MS4A6A reduced endothelial dysfunction and monocyte adhesion, decreasing the expression of inflammatory factors, adhesion molecules, and reactive oxygen species (ROS). The pathway inhibitor Bay 11-7085 (irreversible inhibitor of IxBalpha phosphorylation) using IκB kinase (IKK) silencing showed that MS4A6A promotes endothelial dysfunction and monocyte adhesion by regulating the IKK/NF-kappaB pathway. This study demonstrated for the first time that MS4A6A facilitates endothelial dysfunction and monocyte adhesion by modulating the IKK/NF-κB signaling pathway, thereby promoting the progression of AS. This study provides a theoretical foundation for utilizing MS4A6A as a biomarker and potential therapeutic target for the prevention and treatment of AS.