OLR1 is a cell-surface endocytosis receptor that binds to oxLDL, a marker of atherosclerosis. The binding of oxLDL to OLR1 induces vascular endothelial cell activation and dysfunction, leading to pro-inflammatory responses, oxidative stress, and apoptosis . This receptor is involved in the regulation of Fas-induced apoptosis and may play a role as a scavenger receptor .
The expression of OLR1 is regulated through the cyclic AMP signaling pathway. Under normal conditions, the expression of LOX-1 on endothelial cells is low. However, it is significantly upregulated by various atherosclerotic stimuli such as tumor necrosis factor-alpha, oxLDL, and blood vessel shear stress . Other ligands for LOX-1 include oxidized high-density lipoprotein, advanced glycation end-products, platelets, and apoptotic cells .
Mutations in the OLR1 gene have been associated with several cardiovascular diseases, including atherosclerosis and myocardial infarction . The receptor’s role in endothelial dysfunction and plaque formation contributes to the initiation, progression, and destabilization of atheromatous plaques, which can lead to myocardial infarction and certain forms of stroke . Additionally, OLR1 may modify the risk of Alzheimer’s disease .
Given its significant role in cardiovascular diseases, OLR1 is a target of interest for therapeutic interventions aimed at reducing atherosclerosis and its associated complications. Research is ongoing to develop inhibitors that can block the interaction between oxLDL and LOX-1, potentially mitigating the pro-atherogenic effects of oxLDL .