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
- Global aging has led to a steady rise in the number of older adults suffering from the first-episode depression with cognitive impairment (FEDCI), which imposes a huge medical and financial burden on patients and their families. The aim of this study was to explore the influence of the NOS3 rs1799983 polymorphism on the FEDCI. - Source: PubMed
Publication date: 2026/02/03
Yin YinaTang LingkaiXia JiaojiaoChang JunxiaoQian MinChen FeifeiLi ShumingGu Xiaoping - This study aims to elucidate the multi-target molecular mechanism of cyanidin-3-O-glucoside (C3G) in treating Type 2 Diabetes (T2DM) through network pharmacology methods. - Source: PubMed
Publication date: 2026/04/08
Yang WenlingWu MeizhenLuo JuanlieLi YaohuaPan XiaojiaoTian Hui - RNA interference (RNAi) of the placental glucose transporter SLC2A3 resulted in smaller hypoglycemic fetuses with reduced umbilical artery insulin and glucagon concentrations at mid-gestation (75 days of gestation [dGA]) in sheep. Our current objective was to determine the ramifications of SLC2A3-RNAi throughout gestation, and to assess fetal insulin secretion in response to glucose and arginine challenges. We successfully generated SLC2A3-RNAi (n = 6) and NTS-RNAi (non-targeting sequence) control sheep pregnancies (n = 6). Near-term they underwent surgical catheterization followed by in vivo metabolic studies at 133 ± 2 dGA. A baseline metabolic study, which included assessment of uterine and umbilical blood flow rates, was followed by a square-wave hyperglycemic clamp of the fetus (GSIS), followed by infusion of an arginine bolus to assess maximal fetal insulin secretion. The baseline metabolic study determined that uterine glucose uptake (mmol/min) was reduced 29% (P = 0.03), as was placental glucose utilization by 40% (P = 0.05), but umbilical glucose uptake was not impacted in SLC2A3-RNAi pregnancies. By contrast, amino acid carbon uptake/kg of uterus increased 76%, as did placental utilization of amino acid carbon (P = 0.09), indicating placental compensation supported by increased mRNA concentrations of NOS3, IGF2, IGF1R and IGF2R (P ≤ 0.05 to ≤ 0.10). Unlike the findings at 75 dGA, near-term fetal body and pancreas weights were no longer significantly (P ≥ 0.10) impacted by SLC2A3-RNAi. While baseline umbilical artery concentrations of glucose and insulin were not different (P ≥ 0.10), two-way ANOVA revealed a significant (P ≤ 0.01) SLC2A3-RNAi treatment effect during GSIS and arginine stimulated insulin secretion (ASIS), demonstrating significant enhancement of fetal insulin secretion capacity. In summary, placental compensatory mechanisms appeared to rescue fetal growth and umbilical glucose concentrations between mid-gestation and near-term. Decreasing placental glucose utilization while increasing amino acid utilization may be a mechanism aiding recovery of glucose transfer to the fetus. While microvillous glucose uptake to the placenta appears to be rate-limiting to fetal growth and development early in gestation, placental glucose transfer and fetal growth are rescued later in gestation. However, increased nutrient stimulated fetal insulin secretion persists near-term, as a possible sequela of the earlier impacts. - Source: PubMed
Publication date: 2026/04/10
Kennedy Victoria CTanner Amelia RLynch Cameron SWinger Quinton ARozance Paul JAnthony Russell V - Repeated low-level red-light (RLRL) therapy effectively controls myopia, yet its retinal metabolic mechanisms remain elusive. This study aimed to elucidate RLRL-induced metabolic alterations in a lens-induced myopia (LIM) chick model. - Source: PubMed
Publication date: 2026/03/21
He ChengjieHuang YanjingZhang ShiranLi JingniLiang JiangboPeng JingyiWu YueHong YingZheng Ying-FengHe Mingguang - Preeclampsia (PE) is a potentially life-threatening multisystem disorder affecting maternal and fetal health and is associated with impaired angiogenesis, endothelial dysfunction, inflammation, and apoptosis. In this study, we characterized molecular, histopathological, and clinical alterations in placentas from 30 women with PE compared with 30 normotensive controls. Placental tissues underwent macroscopic evaluation, histopathology, immunohistochemistry for α-Klotho, endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), placental growth factor (PlGF), and tumor necrosis factor-α (TNF-α), alongside TUNEL assay for apoptosis. PE pregnancies were associated with earlier delivery, lower neonatal birth weight, reduced placental weight and volume, and decreased maternal total protein and albumin levels. Histologically, PE placentas exhibited increased syncytial knots, intervillous fibrin deposition, distal villous hypoplasia, chorangiosis, avascular villi, and calcifications. Immunohistochemical analyses indicated reduced expression of α-Klotho, eNOS, VEGF, and PlGF, with increased TNF-α expression and higher apoptotic index. α-Klotho expression correlated positively with angiogenic markers, placental weight, and birth weight, and negatively with TNF-α and apoptosis. Multivariate regression analyses suggested that PE is associated with increased placental apoptosis and TNF-α expression, as well as reduced α-Klotho, eNOS, VEGF, and PlGF expression, and with lower birth weight, primarily mediated by prematurity. Early-onset PE exhibited more pronounced α-Klotho reduction with relatively preserved eNOS expression, suggesting potential compensatory endothelial responses, while magnesium sulfate or antihypertensive therapy did not significantly influence molecular profiles. These findings suggest that PE is linked to coordinated alterations in angiogenic, endothelial, and inflammatory pathways associated with placental structural changes and adverse perinatal outcomes. Observed alterations in α-Klotho and angiogenic markers highlight potential pathways for further investigation into targeted molecular interventions. This study is limited by its single-center, and relatively small sample size, which may limit generalizability, and causal relationships cannot be established; further multi-center prospective studies are warranted. - Source: PubMed
Publication date: 2026/04/10
Gelenli Dolanbay ElifHocaoglu MeryemMert TugayInan Gungor HacerCalıskan Bender GozdeOzkanli SeymaAnkarali HandanAyaz Bilir ReyhanKomurcu Zeynep NurDokmeci Guney DamlaTurgut AbdulkadirUslu Unal