|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
The eNOS G894T polymorphism may play role in the endothelial dysfunction observed during acute PUUV infection.
|
26561052 |
2015 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
The aim of this study was to test the hypothesis that inflammatory cytokines impairs endothelium-dependent relaxation and NO production gets vitiated due to eNOs Glu298Asp gene polymorphism causing endothelial dysfunction in eclampsia.
|
22958187 |
2013 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
Association of endothelial dysfunction with endothelin, nitric oxide and eNOS Glu298Asp gene polymorphism in coronary artery disease.
|
22045428 |
2011 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
In a population with a compromised endothelial function, concentrations of phenols in dietary VOO interact with NOS3 Glu298Asp to ameliorate the endothelial dysfunction associated to the TT genotype.
|
21816783 |
2011 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
Polymorphisms in the endothelial nitric oxide synthase ( eNOS ) gene (- 786T > C and 894G > T ) enhance endothelial dysfunction and have been studied in relation to coronary artery disease (CAD).
|
20846926 |
2010 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
The aim of this study was to test the hypothesis that (i) endothelial nitric oxide (NO) synthase Glu298Asp gene polymorphism limits constitutive NO production causing endothelial dysfunction and (ii) inflammatory cytokines impairs endothelium dependent relaxation in pre-eclampsia.
|
20047583 |
2010 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D, angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED).
|
17504188 |
2007 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
Genetic polymorphism G894T on endothelial nitric oxide synthase (eNOS) gene has been associated with endothelial dysfunction in young smokers, but its role in the pathogenesis of MI is obscure.
|
16337503 |
2006 |
|
rs1799983
|
|
|
0.090 |
GeneticVariation |
BEFREE |
The 894T allele of a G894T polymorphism in the endothelial nitric oxide synthase (eNOS) gene is associated with decreased eNOS activity, cleavage of the protein, and endothelial dysfunction.
|
11668050 |
2001 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
It was aimed to explain the association of the endothelial dysfunction, which is thought to play a role in the pathophysiology of CSX, with C677T polymorphism on MTHFR gene based on genetic basis.
|
28481466 |
2018 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
Also, no association between the MTHFR 677 C>T polymorphism and CV events or endothelial dysfunction was observed.
|
20423475 |
2010 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
Angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphisms are linked to endothelial dysfunction and to cerebral white matter lesions.
|
19298544 |
2009 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
Coexistence of homozygosity for the C677T mutation and B12 deficiency is associated with endothelial dysfunction and can be corrected with vitamin B12 and folic acid treatment.
|
17449548 |
2007 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D, angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED).
|
17504188 |
2007 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
A slight chronic hypoperfusion or an endothelial dysfunction associated with unfavorable genetic variations such as methylenetetrahydrofolate reductase C677T variation and angiotensin-converting enzyme I/D polymorphism then may lead indirectly to a malfunction of the molecular cross-talk between the nucleus and the mitochondria.
|
17114822 |
2007 |
|
rs1217691063
|
|
|
0.070 |
GeneticVariation |
BEFREE |
C677T polymorphism in methylenetetrahydrofolate reductase gene (MTHFR) is a major determinant of hyperhomocysteinemia, which results in endothelial dysfunction.
|
15226090 |
2004 |
|
rs72551362
|
|
|
0.030 |
GeneticVariation |
BEFREE |
Endothelial dysfunction in angiotensin II-treated E-V290M vasopressin-exposed offspring was attenuated by tempol, an effect which was more prominent in male offspring.
|
31104564 |
2019 |
|
rs72551362
|
|
|
0.030 |
GeneticVariation |
BEFREE |
Endothelial dysfunction in the basilar artery from E-V290M mice fed low salt was attenuated by scavengers of superoxide, inhibitors of NADPH oxidase, or blockade of the Ang II AT1 (angiotensin type-1) receptor.
|
30354810 |
2018 |
|
rs72551362
|
|
|
0.030 |
GeneticVariation |
BEFREE |
Conversely, IL-1β-induced endothelial dysfunction was worsened in the aorta from E-V290M mice.
|
26566726 |
2016 |
|
rs5742905
|
|
|
0.020 |
GeneticVariation |
BEFREE |
We found that, compared with untreated I278T mice, OT-58 treatment of I278T mice fed with the REG diet resulted in a 90% decrease in plasma Hcy concentrations and correction of learning/cognition, endothelial dysfunction, hemostasis, bone mineralization, and body composition.
|
31450979 |
2019 |
|
rs876657421
|
|
|
0.020 |
GeneticVariation |
BEFREE |
We found that, compared with untreated I278T mice, OT-58 treatment of I278T mice fed with the REG diet resulted in a 90% decrease in plasma Hcy concentrations and correction of learning/cognition, endothelial dysfunction, hemostasis, bone mineralization, and body composition.
|
31450979 |
2019 |
|
rs5742905
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Tg-I278T Cbs(-/-) mice exhibited severe hyperhomocysteinemia and endothelial dysfunction in cerebral arterioles.
|
22186991 |
2012 |
|
rs876657421
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Tg-I278T Cbs(-/-) mice exhibited severe hyperhomocysteinemia and endothelial dysfunction in cerebral arterioles.
|
22186991 |
2012 |
|
rs4961
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Since inflammatory mechanisms may be involved in pathophysiology of hypertension and in endothelial dysfunction and atherosclerosis through reactive oxygen species, the baseline urinary excretion of inflammatory and oxidative stress markers in a subgroup of adolescents stratified according to <i>ADD1</i>(alpha adducin) rs4961 genotypes was assessed.
|
31760884 |
2020 |
|
rs910042982
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Endothelial dysfunction in angiotensin II-treated E-V290M vasopressin-exposed offspring was attenuated by tempol, an effect which was more prominent in male offspring.
|
31104564 |
2019 |