CCL2 and endothelial dysfunction: More specifically, such a nexus is controlled by a multitude of factors, including (1) endothelial dysfunction, (2) elevation in the rates of TNF-α, IL-6, MCP-1 (monocyte chemoattractant protein-1), and C-reactive protein (CRP), (3) enhanced levels of metalloproteinases in extracellular vesicles (EVs), (4) triggered asymmetric dimethylarginine, and (5) decreased levels of adipokine (particularly, adiponectin).