ArticleExperimental & molecular medicine2010
Genistein activates endothelial nitric oxide synthase in broiler pulmonary arterial endothelial cells by an Akt-dependent mechanism.
Article in Experimental & molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 33 citations in OpenAlex.
- Immune modulation by sex hormones: unveiling the complex interplay and regulatory networks.Frontiers in immunology · 2026Review
- Genistein Restores Nitric Oxide Bioavailability and Attenuates Oxidative Stress in Angiotensin II-Induced Hypertensive Mice.Preventive nutrition and food science · 2026Article
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Replacing Hydrolyzed Soybean Meal with Recombinant β-Glucosidase Enhances Resistance toInternational journal of molecular sciences · 2024Article
- Natural Products for the Treatment of Pulmonary Hypertension: Mechanism, Progress, and Future Opportunities.Current issues in molecular biology · 2023Review
- Canagliflozin ameliorates renal oxidative stress and inflammation by stimulating AMPK-Akt-eNOS pathway in the isoprenaline-induced oxidative stress model.Scientific reports · 2020Article
- Canagliflozin attenuates isoprenaline-induced cardiac oxidative stress by stimulating multiple antioxidant and anti-inflammatory signaling pathways.Scientific reports · 2020Article
- Systematic Elucidation of the Mechanism of Genistein against Pulmonary Hypertension via Network Pharmacology Approach.International journal of molecular sciences · 2019Article
- Comparative Circadian Metabolomics Reveal Differential Effects of Nutritional Challenge in the Serum and Liver.The Journal of biological chemistry · 2016Article
- Flavonoids in modulation of cell survival signalling pathways.Genes & nutrition · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulation of endothelial nitric oxide synthase (eNOS) plays an important role in the development of multiple cardiovascular diseases. Our recent study demonstrated that genistein supplementation attenuates pulmonary arterial hypertension in broilers by restoration of endothelial function. In this study, we investigated the molecular mechanism by using broiler pulmonary arterial endothelial cells (PAECs). Our results showed that genistein stimulated a rapid phosphorylation of eNOS at Ser(1179) which was associated with activation of eNOS/NO axis. Further study indicated that the activation of eNOS was not mediated through estrogen receptors or tyrosine kinase inhibition, but via a phosphatidylinositol 3-kinase (PI3K)/Akt-dependent signaling pathway, as the eNOS activity and related NO release were largely abolished by pharmacological inhibitors of PI3K or Akt. Thus, our findings revealed a critical function of Akt in mediating genistein-stimulated eNOS activity in PAECs, partially accounting for the beneficial effects of genistein on the development of cardiovascular diseases observed in animal models.
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