Sanjiv Singh1, Avtar Singh Gautam2. 1. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Export Promotions Industrial Park (EPIP), Industrial Area, Hajipur, Dist: Vaishali, Bihar, 844102, India. sanjivpg2006@yahoo.com. 2. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Export Promotions Industrial Park (EPIP), Industrial Area, Hajipur, Dist: Vaishali, Bihar, 844102, India.
Abstract
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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.
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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.
Authors: L Cominacini; A F Pasini; U Garbin; A Davoli; M L Tosetti; M Campagnola; A Rigoni; A M Pastorino; V Lo Cascio; T Sawamura Journal: J Biol Chem Date: 2000-04-28 Impact factor: 5.157
Authors: H Kataoka; N Kume; S Miyamoto; M Minami; H Moriwaki; T Murase; T Sawamura; T Masaki; N Hashimoto; T Kita Journal: Circulation Date: 1999-06-22 Impact factor: 29.690