CCL2 and endothelial dysfunction: It is well known that in the early stages of the atherosclerotic process, endothelial dysfunction leads to the production of increased quantities of inflammatory cytokines (IL1β, IL6, CRP, MCP-1—monocyte chemoattractant protein-1), proteases (matrix metalloproteinase—MMP), extracellular vesicles, and adhesion molecules (P-selectin, E-selectin, ICAM—Intracellular Adhesion Molecule, VCAM—Vascular Cell Adhesion Molecule), which contributes to monocyte attraction and is secondary to intima infiltration.