ArticleOxidative medicine and cellular longevity2018
Nrf2 Deficiency Unmasks the Significance of Nitric Oxide Synthase Activity for Cardioprotection.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Combination of genetic eNOS deficiency and high-fat diet induces reproducible cardiometabolic HFpEF.Redox biology · 2026Article
- Green-Synthesized Silver Nanoparticles fromAntioxidants (Basel, Switzerland) · 2026Article
- NRF2-Targeted Therapy in Cardiovascular Disease Transitions from Systemic Activation to Precision Redox Medicine.Antioxidants (Basel, Switzerland) · 2026Review
- Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases.Redox biology · 2025Review
- Acute blood loss anemia aggravates endothelial dysfunction after acute myocardial infarction.Frontiers in cardiovascular medicine · 2025Article
- Upregulation of Nrf2 in myocardial infarction and ischemia-reperfusion injury of the heart.PloS one · 2024Article
- Advances in Understanding the Role of NRF2 in Liver Pathophysiology and Its Relationship with Hepatic-Specific Cyclooxygenase-2 Expression.Antioxidants (Basel, Switzerland) · 2023Review
- The P21-Activated Kinase 1 and 2 As Potential Therapeutic Targets for the Management of Cardiovascular Disease.International journal of drug discovery and pharmacology · 2022Article
- Red blood cell eNOS is cardioprotective in acute myocardial infarction.Redox biology · 2022Article
- Cigarette smoke-induced oxidative stress activates NRF2 to mediate fibronectin disorganization in vascular formation.Open biology · 2022Article
- Sulforaphane alleviates hypoxic vestibular vertigo (HVV) by increasing NO production via upregulating the expression of NRF2.Bioengineered · 2022Article
- Systems redox biology in health and disease.EXCLI journal · 2022Review
- Pak2 Regulation of Nrf2 Serves as a Novel Signaling Nexus Linking ER Stress Response and Oxidative Stress in the Heart.Frontiers in cardiovascular medicine · 2022Article
- The Antioxidant Transcription Factor Nrf2 in Cardiac Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Review
- Red Blood Cell and Endothelial eNOS Independently Regulate Circulating Nitric Oxide Metabolites and Blood Pressure.Circulation · 2021Article
- Cardiac Protection by Oral Sodium Thiosulfate in a Rat Model of L-NNA-Induced Heart Disease.Frontiers in pharmacology · 2021Article
- The epitranscriptomic writer ALKBH8 drives tolerance and protects mouse lungs from the environmental pollutant naphthalene.Epigenetics · 2020Article
- Tsg101 positively regulates P62-Keap1-Nrf2 pathway to protect hearts against oxidative damage.Redox biology · 2020Article
- The Dark Side of Nrf2 in the Heart.Frontiers in physiology · 2020Review
- Real-Ambient Particulate Matter Exposure-Induced Cardiotoxicity in C57/B6 Mice.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a key master switch that controls the expression of antioxidant and cytoprotective enzymes, including enzymes catalyzing glutathione de novo synthesis. In this study, we aimed to analyze whether Nrf2 deficiency influences antioxidative capacity, redox state, NO metabolites, and outcome of myocardial ischemia reperfusion (I/R) injury. In Nrf2 knockout (Nrf2 KO) mice, we found elevated eNOS expression and preserved NO metabolite concentrations in the aorta and heart as compared to wild types (WT). Unexpectedly, Nrf2 KO mice have a smaller infarct size following myocardial ischemia/reperfusion injury than WT mice and show fully preserved left ventricular systolic function. Inhibition of NO synthesis at onset of ischemia and during early reperfusion increased myocardial damage and systolic dysfunction in Nrf2 KO mice, but not in WT mice. Consistent with this, infarct size and diastolic function were unaffected in eNOS knockout (eNOS KO) mice after ischemia/reperfusion. Taken together, these data suggest that eNOS upregulation under conditions of decreased antioxidant capacity might play an important role in cardioprotection against I/R. Due to the redundancy in cytoprotective mechanisms, this fundamental antioxidant property of eNOS is not evident upon acute NOS inhibition in WT mice or in eNOS KO mice until Nrf2-related signaling is abrogated.
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