ArticlePloS one2014
Adenovirus-mediated eNOS expression augments liver injury after ischemia/reperfusion in mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Splenectomy reduces shear stress and inflammation in liver endothelial cells during regeneration after partial hepatectomy in mice.Scientific reports · 2025Article
- Mechanism of Reactive Oxygen/Nitrogen Species in Liver Ischemia-Reperfusion Injury and Preventive Effect of Chinese Medicine.Chinese journal of integrative medicine · 2025Review
- miR-486-5p protects against rat ischemic kidney injury and prevents the transition to chronic kidney disease and vascular dysfunction.Clinical science (London, England : 1979) · 2024Article
- New progress in understanding roles of nitric oxide during hepatic ischemia-reperfusion injury.World journal of hepatology · 2022Review
- Restraint Stress Alters Expression of Glucocorticoid Bioavailability Mediators, Suppresses Nrf2, and Promotes Oxidative Stress in Liver Tissue.Antioxidants (Basel, Switzerland) · 2020Article
- The protective effect of bone marrow-derived mesenchymal stem cells in liver ischemia/reperfusion injury via down-regulation of miR-370.Iranian journal of basic medical sciences · 2019Article
- New progress in roles of nitric oxide during hepatic ischemia reperfusion injury.World journal of gastroenterology · 2017Review
- Protective effect of eNOS overexpression against ischemia/reperfusion injury in small-for-size liver transplantation.Experimental and therapeutic medicine · 2016Article
- Antitumoral gene-based strategy involving nitric oxide synthase type III overexpression in hepatocellular carcinoma.Gene therapy · 2016Article
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
Hepatic ischemia/reperfusion (l/R) injury continues to be a critical problem. The role of nitric oxide in liver I/R injury is still controversial. This study examines the effect of endothelial nitric oxide synthase (eNOS) over-expression on hepatic function following I/R. Adenovirus expressing human eNOS (Ad-eNOS) was administered by tail vein injection into C57BL/6 mice. Control mice received either adenovirus expressing LacZ or vehicle only. Sixty minutes of total hepatic ischemia was performed 3 days after adenovirus treatment, and mice were sacrificed after 6 or 24 hrs of reperfusion to assess hepatic injury. eNOS over expression caused increased liver injury as evidenced by elevated AST and ALT levels and decreased hepatic ATP content. While necrosis was not pervasive in any group, TUNEL demonstrated significantly increased apoptosis in Ad-eNOS infected livers. Western blotting demonstrated increased levels of protein nitration and upregulation of the pro-apoptotic proteins bax and p53. Our data suggest that over-expression of eNOS is detrimental in the setting of hepatic I/R.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.