The involvement of LOX-1 is a factor that affects development of atherosclerosis from several factors; for example, dyslipidemia played the major role in the upregulation of LOX-1 through ox-LDL stimulation [19], hyperglycemia increased LOX-1 upregulation in human endothelial cells via activation of reactive oxygen species (ROS) [20], and hypertension upregulated the expression of LOX-1 by induction of angiotensin II [21]. Here, OLR1 is linked to metabolic syndrome.