CCL2 and atherosclerosis: By binding to their cell surface receptor (RAGE) on macrophages and endothelial cells, AGEs trigger a cascade of ROS generation and activation of proinflammatory pathways and profibrotic factors such as nuclear factor-κB (NF-κB), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), plasminogen activator inhibitor-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) involved in the progression of atherosclerosis and vascular pathology [33].