LOX-1 is a class E scavenger receptor that mediates the uptake of oxLDL by vascular cells. LOX-1 is involved in endothelial dysfunctions, monocyte adhesion, the proliferation, migration, and apoptosis of smooth muscle cells, foam cell formation, platelet activation, as well as plaque instability; all of these events are critical in the pathogenesis of atherosclerosis.
These LOX-1-dependent biological processes contribute to plaque instability and the ultimate clinical sequelae of plaque rupture and life-threatening tissue ischemia.
Administration of anti-LOX-1 antibodies inhibits atherosclerosis by decreasing these cellular events. Over the past decade, multiple drugs including naturally occurring antioxidants, statins, anti-inflammatory agents, antihypertensive and antihyperglycemic drugs have been demonstrated to inhibit vascular LOX-1 expression and activity. Therefore, LOX-1 represents an attractive therapeutic target for the treatment of human atherosclerotic diseases.
LOX-1 identified as the primary receptor for oxLDL uptake by endothelial cells (EC). LOX-1 is also expressed by monocytes/macrophages, smooth muscle cells(SMC), cardiomyocytes, fibroblasts, adipocytes, airway epithelial cells and platelets.
Like CD36, LOX-1 acts as a cell surface SR that participates in the binding, endocytosis, and proteolytic degradation  of oxLDL.
Soluble LOX-1(sLOX-1), a fragment of the main LOX-1 molecule, is being investigated as a diagnostic marker because it has been shown to be present in increased quantities in patients with hypertension, diabetes, metabolic syndrome and coronary artery disease.