This is related to endothelial dysfunction modulated by cell adhesion molecules, such as E-selectin, leukocyte recruitment and binding dysfunction, macrophage migration alteration, smooth muscle cell proliferation, increased production of angiotensin II, PAI-1, free fatty acids, and AGEs, and increased lipid oxidation, which will result in the further release of proinflammatory cytokines [30,47,48,49,50,51]. Here, SELE is linked to endothelial dysfunction.