GPR182 promotes atherosclerosis via facilitating arterial lipid deposition
Elevated circulating low-density lipoprotein cholesterol (LDL-C) is a primary risk factor for atherosclerosis; however, the molecular mechanisms underlying lipid plaque formation within the artery wall remain poorly understood. Here, we identify GPR182, a recently characterized lipoprotein receptor of the atypical chemokine receptor family, as a key mediator of lipid deposition in the aortic…
Elevated LDL-C is a well-known risk factor for atherosclerosis; however, the molecular mechanisms behind lipid plaque formation within artery walls are not yet fully understood. Researchers have now identified GPR182, an atypical chemokine receptor, as a key player in lipid deposition in aortic endothelium during atherosclerosis.
Depleting GPR182 genetically offers protection against atherosclerosis in various mouse models, without affecting cholesterol levels or immune cell recruitment to plaques. GPR182 is expressed by aortic endothelial cells and is upregulated during disease progression. This receptor aids in LDL uptake by aortic ECs, both in lab settings and in living organisms.
Inhibiting GPR182 using a monoclonal antibody reduces lipid uptake in the aorta and slows down disease progression when cholesterol levels are high. These findings highlight the crucial role of endothelial GPR182 in aortic lipid deposition and plaque formation, suggesting that GPR182 inhibition could be a promising approach for treating atherosclerotic cardiovascular disease.
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