Upon binding to LOX-1, oxLDL induced the expression of adhesion molecules [62] and monocyte chemoattractant protein-1 (MCP-1) [24] and promoted the production of reactive oxygen species (ROS), NF-κB activation [25, 27, 63], and apoptosis [23], all of which characterized the endothelial dysfunction, a crucial early step in atherosclerosis [22, 26]. Here, CCL2 is linked to atherosclerosis.