It directly induces vascular injury and endothelial dysfunction, which involves increased systemic vasoconstrictors, including ET-1, tumor necrosis factor α, C-reactive protein, prostaglandin E2, and interleukin 1β, elevated pro-inflammatory factors and adhesion molecules such as interleukin 6, monocyte chemoattractant protein 1, E-selectin, VCAM-1, ICAM-1, soluble vascular cellular adhesion molecule 1 and soluble intercellular adhesion molecule 1sICAM-1, and pro-thrombosis, involving the von Willebrand factor and tissue factor [57,58]. Here, SELE is linked to endothelial dysfunction.