In a randomly sampled cross-sectional study of 985 South Asian, Chinese, and European Canadians, three common isoforms of ApoE (E2, E3 and E4), plasma lipid concentrations and atherosclerosis of the carotid artery were measured.
Among 1677 nondemented ARIC (Atherosclerosis Risk in Communities) participants (mean age=76±5 years; 40% men; 26% black) with 3-Tesla MRI scans at the fifth examination (2011-2013), we fit multinomial logistic regression models to quantify relationships of brain volumes (Alzheimer disease signature regions, total gray matter, frontal gray matter, and white matter hyperintensity volumes), infarct frequencies (lacunar, nonlacunar, and total), and apolipoprotein E (number of ε4 alleles) with CMB location (none, deep/mixed, or strictly lobar CMBs).
Previous studies suggest that klotho gene polymorphisms may be associated with atherosclerosis, but did not assess the relationship between klotho gene polymorphisms and atherosclerosis parameters such as carotid artery intima-media thickness (IMT).
In this study, we evaluated the effects of complete IL-25 deficiency or of a temporal IL-25 blockade on atherosclerosis development in apolipoprotein E-deficient (<i>Apoe</i><sup>-/-</sup>) mice.
We recently described that apolipoprotein E (ApoE) deficient mice with a mutation in the fibrillin-1 (Fbn1) gene (ApoE<sup>-/-</sup>Fbn1<sup>C1039G+/-</sup>) develop accelerated atherosclerosis, plaque rupture, myocardial infarction, cerebral hypoxia and sudden death.
Clinical and autoptical studies have suggested a predisposing role of the allele E4 of apolipoprotein E (apoE) in the development of atherosclerosis and cardiovascular disease.
The molecular polymorphism displayed by apolipoprotein E (apoE, protein; APOE, gene) has been listed as a risk factor for susceptibility to various disorders, such as those associated with lipid metabolism and arteriosclerosis.
Beyond the known influence of ApoE polymorphisms on serum lipid profile, the pathogenesis of atherosclerosis, and the development of neurodegenerative disorders, ApoE also has a major role in the pathogenesis and progression of a variety of renal diseases, as well as in the atherosclerotic complications associated with them.
These findings support the proposal that common genetic variations in the eNOS gene contribute to atherosclerosis susceptibility, presumably by effects on endothelial NO availability.
In conclusion, the homozygous NOS III variant (GG) status does not seem to interact additively with the ACE homozygous DD genotype in determining flow-mediated vasodilation in individuals with established atherosclerosis and pre-existent endothelial dysfunction.
The objective of this study was to investigate the influence of the APOE promoter (-491 A/T, -427 T/C and -219 G/T) and coding region (APOE epsilon2/epsilon3/epsilon4) polymorphisms in atherosclerosis disease by association and linkage disequilibrium analyses.
It was the objective of this study to investigate the relation between nitric oxide synthase (NOS3) gene polymorphisms, vascular inflammation, endothelial function, and atherosclerosis.
As atherosclerosis is provoked by both inflammation and hyperlipidemia, we aimed to determine the effect of inulin supplementation on atherosclerosis development in hypercholesterolemic <i>APOE*3-Leiden</i> (<i>E3L</i>) mice.
In the present study, we analyzed the G894T polymorphism of the eNOS gene in groups of individuals diagnosed with atherosclerosis and in a control group.
Independent effects of the -219 G>T and epsilon 2/ epsilon 3/ epsilon 4 polymorphisms in the apolipoprotein E gene on coronary artery disease: the Southampton Atherosclerosis Study.
The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.
In Gbeta3 polymorphism, the 825T allele carriers had a significantly lower body mass index while in eNOS polymorphism there were no links between genotypes, renal function and atherosclerosis risk factors.
Since nuclear factor-κB (NF-κB) is a central regulator of inflammatory processes, we hypothesized that chronically enhanced hepatic NF-κB activation, through hepatocyte-specific expression of IκB kinase-β (IKKβ) (LIKK), will aggravate atherosclerosis development in APOE*3-Leiden (E3L) mice.