title: An oxidized low-density lipoprotein receptor gene variant is inversely associated with the severity of coronary artery disease.
abstract: BACKGROUND
  A lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1) is the major receptor of oxidized LDL in endothelial cells. The expression of LOX-1 was shown to be upregulated in atherosclerotic lesions. Recently, LOX-1 gene polymorphism (G501C) was reported to be associated with myocardial infarction (MI).
  
  
  OBJECTIVE
  Our study was undertaken to elucidate the association between this polymorphism and coronary artery disease (CAD).
  
  
  METHODS
  We evaluated LOX-1 gene polymorphism using Invader assay in 586 patients undergoing coronary angiography.
  
  
  RESULTS
  Study patients were categorized into three groups: normal/minimal stenosis (< or =25%) (n = 128); mild stenosis (26-50%) (n = 39); and significant stenosis (>50%) (n = 419). Of the 419 patients with significant stenosis, 163 had single-vessel, 165 had double-vessel, and 91 had triple-vessel disease. Myocardial infarction was present in 171 patients. The frequency of LOX- 1 gene variants (C/C or C/G) was lower in patients with significant than in those with normal/minimal stenosis (36 vs. 49%, p < 0.01). The frequency of LOX-1 gene variants did not differ between patients with and without MI (34 vs. 37%). However, a stepwise decrease in the frequency of such variants was found depending on the severity of CAD: 49% in normal/minimal stenosis, 41% in mild stenosis, 39% in single-vessel, 35% in double-vessel, and 32% in triple-vessel disease. Multivariate analysis demonstrated LOX-1 gene variants to be inversely associated with the presence of significant stenosis (odds ratio = 0.61; 95% confidence interval = 0.41-0.92).
  
  
  CONCLUSIONS
  The LOX-1 gene variants at 501 were found to be inversely associated with the severity of CAD. This polymorphism may be modifying the severity of CAD.
authors.affiliation: First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
authors.forename: Reiko
authors.initials: R
authors.lastname: Ohmori
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Momiyama
authors.forename: Makoto
authors.initials: M
authors.lastname: Nagano
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Taniguchi
authors.forename: Tohru
authors.initials: T
authors.lastname: Egashira
authors.forename: Atsushi
authors.initials: A
authors.lastname: Yonemura
authors.forename: Haruo
authors.initials: H
authors.lastname: Nakamura
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kondo
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
mesh_terms: D000368:Aged; D008078:Cholesterol, LDL / Q000235:genetics* / Q000502:physiology; D003324:Coronary Artery Disease / Q000235:genetics* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D018110:Receptors, Lipoprotein / Q000235:genetics*
chemical_list: D008078:Cholesterol, LDL; D018110:Receptors, Lipoprotein