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Oxidized low-density lipoprotein receptor 1 (LOX-1) is a type II transmembrane glycoprotein and a member of the class E scavenger receptor family [3, 6]. It serves as the primary receptor for oxidized low-density lipoprotein (oxLDL) in vascular endothelial cells and is also expressed in macrophages, smooth muscle cells, and platelets [4, 7, 13]. Binding of oxLDL to LOX-1 triggers pro-inflammatory and pro-oxidative signaling pathways, such as NF-kappa-B and MAPK, which lead to endothelial dysfunction and the formation of foam cells [1, 4, 9]. These processes are central to the initiation and progression of atherosclerosis and its clinical complications, including myocardial infarction and stroke [3, 14, 16]. Beyond lipid metabolism, LOX-1 is involved in immune responses, including leukocyte adhesion and antigen cross-presentation [9, 12, 17]. Therapeutic interventions targeting LOX-1 include neutralizing antibodies and small molecule inhibitors designed to block oxLDL uptake and downstream signaling [2, 4, 8]. Additionally, existing drugs like statins and aspirin have been shown to indirectly modulate LOX-1 expression and activity [3, 5, 11]. Soluble LOX-1 (sLOX-1), the proteolytically cleaved extracellular domain, is a valuable biomarker for monitoring plaque vulnerability and cardiovascular risk [15, 16].
Inhibition of oxidized low-density lipoprotein binding and downregulation of receptor expression
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