Upregulated LOX-1 Receptor: Key Player of the Pathogenesis of Atherosclerosis.

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In any case, in proatherogenic conditions, LOX-1 is uniquely upregulated in vascular cells and mediates the entire atherogenic process from LDL oxidation to plague arrangement. As evidence supporting the crucial role of LOX-1 in atherogenesis keeps accumulating, there is developing an enthusiasm for LOX-1 as a potential remedial target. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is the major receptor for binding and uptake of oxidized low-density lipoprotein (oxLDL) in endothelial cells. Following internalization of oxLDL, LOX-1 starts a vicious cycle from activation of proinflammatory signaling pathways, subsequently advancing an expanded responsive oxygen species arrangement and secretion of proinflammatory cytokines. In healthy arteries, expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is practically undetectable. This review portrays existing evidence supporting the role of LOX-1 in mediating of proatherosclerotic impacts of oxLDL which result in endothelial dysfunction, proinflammatory recruitment of monocytes into the arterial intima, arrangement of foam cells, endothelial cell dysfunction and vascular smooth muscle cell proliferation, and platelet enactment, angiogenesis just as in plaque development. Likewise, abridges LOX-1 modulatory compounds and in vivo and in vitro examinations toward the improvement of small molecules and biologics that could be of therapeutic use.