Ask about this productRelated genes to: eNOS antibody
- Gene:
- NOS3 NIH gene
- Name:
- nitric oxide synthase 3
- Previous symbol:
- -
- Synonyms:
- ECNOS, eNOS
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-23
- Date modifiied:
- 2016-10-05
Related products to: eNOS antibody
Related articles to: eNOS antibody
- Cardiac fibrosis is a major pathological feature that contributes to the development and progression of heart failure. Endothelial-to-mesenchymal transition (EndMT) is increasingly recognized as an important driver of cardiac fibrosis; however, its regulatory mechanisms remain incompletely understood. Oxytocin (OT) has been reported to exert cardioprotective effects, but whether it modulates EndMT and the underlying signaling pathways requires further investigation. To address this question, a rat model of isoproterenol (ISO)-induced cardiac fibrosis was established. Cardiac structure and function were assessed by echocardiography and histological staining. In vitro, human cardiac microvascular endothelial cells (hCMECs) were stimulated with TGF-β and IL-1β to induce EndMT. Molecular mechanisms were investigated using Western blotting, immunofluorescence, nitric oxide (NO) and cGMP assays, together with pharmacological inhibition and rescue experiments targeting the eNOS/cGMP/PKG signaling pathway. OT markedly attenuated ISO-induced cardiac fibrosis and ameliorated cardiac dysfunction in rats. Moreover, OT suppressed EndMT, as reflected by increased expression of endothelial markers together with reduced expression of mesenchymal markers. Mechanistically, OT enhanced eNOS phosphorylation, increased NO production, and activated downstream cGMP/PKG signaling. Notably, inhibition of cGMP signaling abolished the protective effects of OT, whereas activation of cGMP/PKG rescued EndMT suppression in Nos3-knockdown cells, demonstrating a functional interaction within this pathway. Collectively, these findings indicate that OT mitigates cardiac fibrosis, at least in part, through inhibition of EndMT mediated by activation of the eNOS-cGMP-PKG signaling pathway. This study provides new mechanistic insights into OT-mediated cardioprotection and highlights EndMT and the eNOS/cGMP/PKG axis as potential therapeutic targets for cardiac fibrosis. - Source: PubMed
Publication date: 2026/08/22
Zhao YuFu NaQian XiWang QuanWang ZhuoranWang LingyanFeng RuiWang XiaoyuanQian JinqiaoYang Yuqiao - Coronary artery disease (CAD) is a complex disorder influenced by endothelial dysfunction, vascular inflammation, and thrombosis. This study evaluated selected genetic variants in endothelin signaling (EDN1, PHACTR1), nitric oxide metabolism (NOS3), and fibrinolysis (SERPINE1/PAI-1) in relation to CAD susceptibility, major clinical sub-phenotypes, and disease severity in a Turkish study population. A total of 1256 individuals who underwent coronary angiography were enrolled, including 748 CAD patients and 508 non-CAD controls. Genotyping of EDN1 rs3087459, PHACTR1 rs9349379, NOS3 rs1799983, and PAI-1 4G/5G variants were performed using quantitative real-time PCR. Logistic regression, haplotype, and gene-gene interaction analyses were conducted under multiple inheritance models. The EDN1 CC genotype was significantly associated with CAD (OR = 5.759, 95% CI: 1.319-25.149, p = 0.020), severe CAD (p = 0.012), and C allele with myocardial infarction (OR = 1.640, 95% CI: 1.091-2.465, p = 0.017) in males. Moreover, the PHACTR1 GG genotype was associated with premature CAD (OR = 1.721, 95%CI: 1.076-2.753, p = 0.024), and greater angiographic severity (p < 0.05). The NOS3 T allele carrier males had an increased risk for diabetes (OR = 1.449, 95%CI:1.057-1.985 p = 0.021), and CAD complexed with diabetes (CAD-DM) (OR = 1.619, 95%CI:1.004-2.610, p = 0.048). Notably, the interaction between NOS3 and PHACTR1 variants was consistently associated with CAD, severe CAD, premature CAD, and CAD-DM, and was further supported by higher stenosis severity indices and elevated troponin levels (p < 0.05). These findings demonstrate that variation within endothelial pathways extends beyond CAD susceptibility to shape angiographic complexity and clinical severity. Notably, a synergistic interaction between PHACTR1 and NOS3 modulates CAD related phenotypes, emphasizing that coordinated pathway disturbances contribute to CAD heterogeneity more than isolated variants. - Source: PubMed
Publication date: 2026/08/22
Ozuynuk-Ertugrul Aybike SenaEkici BerkayKocak AjarCoban Neslihan - The aim of this study was to identify genetic variations that influence the metabolic-inflammatory profile of coronavirus disease and to evaluate the performance of modern machine learning models for the classification and prediction of COVID-19 severity. Real-time polymerase chain reaction was used to genotype the polymorphism of FGB (rs1800790), NOS3 (rs2070744) and TMPRSS2 (rs12329760) genes. Model performance was assessed using Accuracy and AUC-ROC, with a focus on maximizing AUC-ROC to ensure optimal discrimination, and SHAP analysis. Optimal hyperparameters for each model were defined as those yielding the highest mean AUC-ROC value during 5-fold cross-validation. COVID-19 severity is strongly associated with a pronounced pro-inflammatory and pro-endothelial activation profile, characterized by significantly elevated transmembrane serine protease 2 (TMPRSS2), endothelin-1 (ET-1), interleukin-6 (IL-6) and procalcitonin (PCT) levels, together with marked metabolic dysregulation. Genetic variations contribute to inter-individual differences in biomarker expression, with specific allelic variants modulating inflammatory intensity and endothelial dysfunction. In particular, the FGB rs1800790 A-allele and eNOS rs2070744 ТТ-genotype are associated with a more pronounced inflammatory response and endothelial dysfunction, while rs12329760 TMPRSS2 variants show weaker but detectable modulatory effects with higher transmembrane serine protease 2 value in T-allele moderate-severe COVID-19 patients. Ensemble methods such as ExtraTreesClassifier (Accuracy: 0.974 ± 0.022) and RandomForestClassifier (Accuracy: 0.960 ± 0.035) demonstrated the highest ROC curves approaching, confirming their encouraging performance in predicting COVID-19 severity. Simpler models, including BernoulliNB (Accuracy: 0.956 ± 0.037) and DecisionTreeClassifier (Accuracy: 0.938 ± 0.043), also showed high classification quality. Analysis of misclassification patterns revealed that ExtraTreesClassifier, HistGradientBoostingClassifier, BaggingClassifier, and GradientBoostingClassifier made no errors across any class. The poorest performance was observed with LinearDiscriminantAnalysis, which generated 11 misclassifications, followed by CalibratedClassifierCV, and LogisticRegressionCV. External validation of the obtained results in larger multicentre cohorts is essential before clinical implementation. - Source: PubMed
Publication date: 2026/08/05
Sydorchuk LarysaSokolenko MaksymSydorchuk RuslanSokolenko AlinaKamyshna IrynaSokolenko LudmilaMoroz PetroSydorchuk AndriiSokolenko OleksandrHalabitska IrynaPetakh PavloKamyshnyi Oleksandr - Pulmonary hypertension (PH) is a common complication of acute exacerbated chronic obstructive pulmonary disease (AECOPD) and is associated with poor prognosis. Nitric oxide synthase (NOS) imbalance may contribute to pulmonary vascular dysfunction, but the clinical value of serum inducible NOS (iNOS), endothelial NOS (eNOS), and the eNOS/iNOS ratio in AECOPD with PH remains unclear. - Source: PubMed
Publication date: 2026/08/18
Zhang YatingZhang DongruiJia WeiLi Yi - Cerebral ischemia/reperfusion injury (CIRI) is a major cause of neurological dysfunction after ischemic stroke, and effective therapies remain limited. Gomisin A, a bioactive lignan isolated from Schisandra chinensis, exhibits antioxidant and anti-apoptotic activities, but its role in CIRI remains unclear. Here, the protective effects of Gomisin A were investigated using middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation/reoxygenation (OGD/R) cell models. Gomisin A significantly reduced cerebral infarct volume and improved neurological outcomes in MCAO rats. In OGD/R models, it enhanced endothelial cell migration and tube formation, accompanied by increased VEGF expression and activation of the VEGF/PI3K/AKT/NOS3 signaling pathway. In addition, Gomisin A alleviated oxidative stress and suppressed apoptosis in both cellular and animal models. Pharmacological inhibition of VEGF with axitinib partially reversed these protective effects, supporting the involvement of VEGF-dependent signaling. Collectively, these findings suggest that Gomisin A exerts neuroprotective effects against CIRI by enhancing angiogenic activity while attenuating oxidative stress and apoptosis, partly through activation of the VEGF/PI3K/AKT/NOS3 pathway. Gomisin A may therefore represent a promising candidate for the treatment of ischemic stroke. - Source: PubMed
Publication date: 2026/08/14
Zhao ChengheYu JiayueLiu KexinWang ShuanglingJing WenpingZhao ZiyiZhuang Wenyue