Oxidized low-density lipoprotein (Ox-LDL) can induce endothelial dysfunction by several mechanisms including (1) binding to scavenger receptors such as receptor-A1, -A2, and lectin-like oxidized low-density lipoprotein receptor (SR-A1, SR-A2, and LOX-1) [44,45]; (2) upregulating the expression of its own receptor LOX-1 on endothelial cells and activating endothelial cells; (3) promoting the growth and migration of smooth muscle cells, monocytes/macrophages and fibroblasts; and (4) leading to oxidative stress through generation of excessive ROS amounts. The gene discussed is OLR1; the disease is endothelial dysfunction.