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Oxidized low-density lipoprotein receptor 1 (LOX-1) is a type II membrane protein, encoded by the OLR1 gene, and is the principal receptor for oxidized LDL (oxLDL) in endothelial cells, macrophages, smooth muscle cells, and several other cell types[1][4][8]. LOX-1 belongs to the C-type lectin-like superfamily and mediates the binding, internalization, and degradation of oxLDL, contributing to the formation of foam cells and vascular dysfunction in atherosclerosis[1][3]. Its expression is highly inducible by atherogenic stimuli (e.g., inflammatory cytokines, hypertension, oxidized lipids, diabetes) and is low under physiological conditions[1][3][5]. LOX-1 also binds other ligands, including apoptotic cells, platelets, advanced glycation end-products, and bacteria[4]. Activation of LOX-1 by oxLDL initiates inflammatory, pro-adhesive, and apoptotic signaling pathways, making it a critical player in endothelial dysfunction and atherogenesis[1][3][4][5]. Soluble LOX-1 can be detected in the circulation and is investigated as a biomarker for cardiovascular disease risk[3]. Targeting LOX-1 is considered a promising therapeutic strategy for the prevention and treatment of cardiovascular and metabolic diseases associated with vascular injury[5].
Inhibition or blockade of LOX-1 reduces oxLDL uptake and foam cell formation, attenuates vascular inflammation, and limits atherosclerotic progression[5]. Downregulation of LOX-1 expression can reduce endothelial dysfunction, apoptosis, and leukocyte adhesion[5][4].
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