LEP and atherosclerosis: On engagement with leptin receptors expressed on vascular cell walls, leptin induces oxidative stress responses, increases MCP-1, TNF-α, IL-6, and endothelin-1, and potentiates proliferation, along with the expression of other endothelial cell adhesion molecules, MMPs, VEGF, and impaired smooth-muscle cell function, resulting in impaired endothelium-dependent vasodilatation promoting hypertension and atherosclerosis [84].