NOS3, nitric oxide synthase 3, 4846

N. diseases: 706; N. variants: 39
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 GeneticVariation phenotype BEFREE Altogether, these data suggest that adult vascular dysfunction in the FGR does not result from early changes in Nos3 promoter DNA methylation, but from an altered vessel structure established during foetal development. 31177629 2019
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype BEFREE Compared with HUVECs from normal newborns, nitric oxide (NO) production was reduced, with imbalance between endothelial nitric oxide synthase (eNOS) and arginase-2 (Arg-2) in IUGR. 30392707 2018
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype BEFREE We tested the hypothesis that melatonin would increase fetal growth in two mouse models of FGR which together represent a spectrum of the placental phenotypes in this complication: namely the endothelial nitric oxide synthase knockout mouse (eNOS<sup>-/-</sup>) which presents with abnormal uteroplacental blood flow, and the placental specific <i>Igf2</i> knockout mouse (P0<sup>+/-</sup>) which demonstrates aberrant placental morphology akin to human FGR. 30158878 2018
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype RGD Arginase upregulation and eNOS uncoupling contribute to impaired endothelium-dependent vasodilation in a rat model of intrauterine growth restriction. 29741931 2018
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype BEFREE The nitric oxide donor 2-[[4-[(nitrooxy)methyl]benzoyl]thio]-benzoic acid methyl ester (SE175) induced significant relaxation of mouse uterine arteries and human placental arteries <i>in vitro</i>; thus, SE175 was encapsulated into these targeted liposomes and administered to healthy pregnant C57BL/6J mice or endothelial nitric oxide synthase knockout (eNOS<sup>-/-</sup>) mice, which exhibit impaired uteroplacental blood flow and FGR. 29109771 2017
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 AlteredExpression phenotype BEFREE Our results indicated that IUGR reduced vasodilation via acetylcholine in aorta rings, decreased NO levels, and increased eNOS phosphorylation at Thr495. 28689502 2017
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype BEFREE We aimed to determine the effects of maternal antioxidant treatment with N-acetylcysteine (NAC) on fetal endothelial function and endothelial nitric oxide synthase (eNOS) programming in IUGR guinea pigs. 27739590 2017
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype CTD_human We hypothesized that treatment of endothelial nitric oxide synthase knockout mice (eNOS⁻/⁻) and catechol-O-methyltransferase knockout mice (COMT⁻/⁻) with resveratrol during pregnancy would improve uterine artery blood flow and therefore ameliorate the PE-like phenotype and FGR in these murine models. 23667712 2013
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 GeneticVariation phenotype BEFREE We analyzed the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene and asymmetric dimethylarginine (ADMA) in 55 Turkish patients with PE without fetal growth retardation (FGR) and in 54 healthy pregnant women. 20598027 2010
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 AlteredExpression phenotype BEFREE Elevated expression of ecNOS was found to be coupled with significantly lower SOD activity and glutathione level, and increased lipid peroxidation in IUGR neonates. 19779107 2009
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype RGD Intrauterine growth restriction and shallower implantation site in rats with maternal hyperinsulinemia are associated with altered NOS expression. 19709742 2009
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 AlteredExpression phenotype BEFREE Normal or IUGR HUVEC monolayers were exposed (0-24h) to 5% O(2) (normoxia), and 1 or 2% O(2) (hypoxia). l-Arginine transport and hCAT-1 expression, phosphorylated and total PKCalpha or eNOS protein and mRNA expression were quantified. eNOS involvement was tested using a siRNA against eNOS (eNOS-siRNA) adenovirus. 19501907 2009
CUI: C0015934
Disease: Fetal Growth Retardation
Fetal Growth Retardation
0.690 Biomarker phenotype HPO