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
- Oxytocin (OT), an endogenous cardiovascular homeostatic hormone, is currently attracting considerable attention because it can improve energy metabolism and cardiac function. This study investigated whether OT mitigates cardiac remodeling in association with alterations in glucose metabolism. In vivo, cardiac hypertrophy and fibrosis were induced in C57BL/6 J mice via angiotensin II (Ang II), while in vitro H9c2 cardiomyoblasts and neonatal rat cardiac fibroblasts (NRCFs) were treated with Ang II or TGF-β1, respectively, with or without OT. We found that OT suppressed cardiac hypertrophy and fibrosis, increased ATP and glucose levels, reduced lactate accumulation, suppressed glycolysis, and enhanced glucose oxidation in cardiomyocytes. Mechanistically, OT upregulated its receptor and inhibited pyruvate kinase M2 (PKM2) in TGF-β1-stimulated NRCFs. In hypertrophic cardiomyocytes induced by Ang II, transcription factor STAT3 was activated and eNOS was downregulated, while OT suppressed STAT3 activation and nuclear translocation of p-STAT3, and enhanced the expression of eNOS. Either Stat3 overexpression or Nos3 downregulation attenuated OT's beneficial and metabolic effects. Additionally, we demonstrated that the transcription factor STAT3 is enriched at and interacts with the Nos3 promoter region. Overexpression of eNOS partially restored OT-associated protective effects that were attenuated by Stat3 overexpression. Collectively, these findings suggest that OT attenuates cardiac remodeling, at least in part, in association with modulation of glucose metabolism and the STAT3/eNOS pathway, providing mechanistic insight into its cardioprotective effects. - Source: PubMed
Publication date: 2026/05/15
Zhao YuQian XiWang QuanWang ZhuoranFu NaWang LingyanFeng RuiYang WeiBai XiangfengQian JinqiaoYang Yuqiao - The aim of this study was to evaluate the nephrotoxicity and molecular mechanism of Evodiamine (EVO). We combined RNA sequencing (RNA-seq) and network toxicology (NT) screening of potential target genes and signaling pathways, used molecular docking to validate core targets, and detected the mRNA expression of the key genes through quantitative real-time polymerase chain reaction (qRT-PCR). After exposure to EVO, body weight of mice decreased significantly, and the levels of renal index, Blood Urea Nitrogen (BUN) and Creatinine (Cr) were significantly increased, with varying degrees of pathological damage to the kidneys. NT identified 125 intersecting targets of EVO exposure related to kidney injury, including AKT1, TNF, TP53, etc. Among the 2888 differentially expressed genes obtained from RNA-seq, 504 genes were up-regulated and 2384 genes were down-regulated. By integrating NT and RNA-seq, 24 intersecting targets were identified. Among them, TRPV1, NOS3, HSP90AA1, and PPARG were selected for molecular docking validation. The results indicated that EVO had the highest affinity for PPARG (-8.07 kcal/mol). The qRT-PCR results indicated that the expression of the and genes was significantly down-regulated, and the expression of the and genes was significantly up-regulated. Immunohistochemistry further confirmed that EVO inhibited the expression of HSP90AA1 and PPARG, while enhancing that of TRPV1 and NOS3. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis suggested that EVO-induced nephrotoxicity is related to signaling pathways such as inflammatory mediator regulation of TRP channels, the PPAR signaling pathway, and the Apelin signaling pathway. In summary, the nephrotoxic effect of EVO may be related to the inhibition of the PPARG signaling pathway, the activation of the TRPV1 channel, the reduction in HSP90AA1 expression, and the imbalance of the Apelin-NOS3 pathway. This study provides a theoretical reference for clarifying the potential mechanism of renal injury caused by EVO and guiding its safe use. - Source: PubMed
Publication date: 2026/04/24
Zhang XuehuaPan YueXiao YuanyuanWu ZiyanYang HuilanLiu YanjunWang YanChen TianqiTang Wenchao - Colorectal cancer (CRC) is a multifactorial disease influenced by genetic and environmental factors. The endothelial nitric oxide synthase (eNOS) gene, involved in nitric oxide (NO) production, is associated with carcinogenesis. This study aimed to evaluate the association between eNOS -786T>C and G894T polymorphisms and CRC susceptibility in an Algerian population. Genotype and allele frequencies were analyzed, and associations were assessed using odds ratios (ORs) and 95% confidence intervals (CIs). For -786T>C polymorphism, the CC genotype was significantly more frequent in patients than in controls (37.33% vs. 21.67%) and was associated with increased risk of CRC (OR = 2.15, 95% CI: 1.21-3.88, = 0.004), whereas the TT genotype showed a protective effect (OR = 0.41, 95% CI: 0.20-0.81, = 0.005). Regarding the G894T polymorphism, the TT genotype was significantly associated with increased susceptibility to CRC (44.67% vs. 8.33%; OR = 8.88, 95% CI: 4.19-15.40, < 0.001), while the GG genotype was protective (OR = 0.18, 95% CI: 0.10-0.32, < 0.001). Allelic analysis confirmed that the C and T alleles were risk factors. Furthermore, eNOS polymorphisms were significantly associated with tumor location. In conclusion, the eNOS -786T>C and G894T polymorphisms are significantly associated with CRC susceptibility in the Algerian population and could serve as potential genetic biomarkers. - Source: PubMed
Publication date: 2026/04/22
Djaballah-Ider Fatma ZohraGouaref InesSeghirate AhlemTouil-Boukoffa ChafiaGalleze Assia - Atherosclerosis (AS) is a major global health burden. Sodium nitrite, a common environmental and dietary contaminant, has been implicated in promoting AS, but its systematic molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/05/05
Yang HaoBoYu YunFengZhang YongHuiBai YaNanShi YaRuJian WeiXiong - Preeclampsia (PE) is the primary cause of maternal and perinatal morbidity and mortality on a global scale. It is driven by a multifactorial aetiology, in which genetic factors involved in blood pressure regulation, including the endothelial nitric oxide synthase () gene, play an important role. This study aimed to investigate the association between gene polymorphisms and the development and severity of PE in an Algerian cohort. - Source: PubMed
Publication date: 2026/03/30
Atmani Sara MimiBouldjennet FaizaKhalili YasmineFeghoul NabylaDammene Debbih Amel