Endothelial dysfunction is a result of changes in endothelial function. Exogenous leptin can promote angiogenesis by increasing vascular endothelial growth factor levels. Macrophages and endothelial cells release nitric oxide. They bind to cells such as fibroblasts, macrophages, endothelial cells, and kidney epithelial cells. SVF includes preadipocytes, fibroblasts, adipose tissue macrophages, and endothelial cells. The gene is expressed in hemopoietic, endothelial, and epithelial cells. VEGF causes a massive signaling cascade in endothelial cells. Basement membrane proteins have been found to accelerate differentiation of endothelial cells. It is required for the selection of endothelial tip and stalk cells during sprouting angiogenesis. This change in the vascular tone is secondary to endothelial dysfunction. Angiopoietin-2 works with VEGF to facilitate cell proliferation and migration of endothelial cells. Magnesium has an indirect antithrombotic effect upon platelets and endothelial function. This occurs by blocking the nucleoside transporter through which adenosine enters erythrocyte and endothelial cells. This reorganization creates intercellular gaps in endothelial cells. They also suppress the proliferation of endothelial cells.