ArticleJournal of the American Heart Association2016
Nitrite Therapy Ameliorates Myocardial Dysfunction via H2S and Nuclear Factor-Erythroid 2-Related Factor 2 (Nrf2)-Dependent Signaling in Chronic Heart Failure.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Cardiac effects of 6 months' dietary nitrate and spironolactone in patients with hypertension and with/at risk of type 2 diabetes, in the factorial design, double-blind, randomized controlled VaSera trial.British journal of clinical pharmacology · 2019Trial
- Bilayer vascular grafts separately loaded with sodium copper chlorophyllin and keratin-based hydrogen sulfide donor with pro-endothelialization, anti-thrombogenicity, anti-inflammation, and anti-calcification properties.Bioactive materials · 2026Article
- Roles of Hydrogen Sulfide (H2S) as a Potential Therapeutic Agent in Cardiovascular Diseases: A Narrative Review.Cureus · 2024Review
- Hydrogen Sulfide and Irisin, Potential Allies in Ensuring Cardiovascular Health.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of long-term inorganic nitrate administration on myocardial ischemia-reperfusion injury in ovariectomized rats.Frontiers in pharmacology · 2024Article
- Anti-oxidant effect of nitrite in the pancreatic islets of type 2 diabetic male rats.Iranian journal of basic medical sciences · 2023Article
- HBiomedicines · 2023Article
- Hydrogen sulfide protects against ischemic heart failure by inhibiting RIP1/RIP3/MLKL-mediated necroptosis.Physiological research · 2022Article
- MLN-4760 Induces Oxidative Stress without Blood Pressure and Behavioural Alterations in SHRs: Roles ofAntioxidants (Basel, Switzerland) · 2022Article
- Long-term inorganic nitrate administration protects against ovariectomy-induced osteoporosis in rats.EXCLI journal · 2022Article
- Itaconate as an inflammatory mediator and therapeutic target in cardiovascular medicine.Biochemical Society transactions · 2021Review
- Nrf2 for cardiac protection: pharmacological options against oxidative stress.Trends in pharmacological sciences · 2021Review
- NRF2 in Cardiovascular Diseases: a Ray of Hope!Journal of cardiovascular translational research · 2021Review
- Hydrogen Sulfide Attenuates Angiotensin II-Induced Cardiac Fibroblast Proliferation and Transverse Aortic Constriction-Induced Myocardial Fibrosis through Oxidative Stress Inhibition via Sirtuin 3.Oxidative medicine and cellular longevity · 2021Article
- HExperimental biology and medicine (Maywood, N.J.) · 2021Article
- Kidney Ischemia-Reperfusion Decreases Hydrogen Sulfide and Increases Oxidative Stress in the Heart.Biomolecules · 2020Article
- Role of Nrf2 and Its Activators in Cardiocerebral Vascular Disease.Oxidative medicine and cellular longevity · 2020Review
- MicroRNA-140-5p aggravates hypertension and oxidative stress of atherosclerosis via targeting Nrf2 and Sirt2.International journal of molecular medicine · 2019Article
- Nrf2 at the heart of oxidative stress and cardiac protection.Physiological genomics · 2018Review
- Hydrogen Sulfide (HFrontiers in pharmacology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBioavailability of nitric oxide (NO) and hydrogen sulfide (H2S) is reduced in heart failure (HF). Recent studies suggest cross-talk between NO and H2S signaling. We previously reported that sodium nitrite (NaNO2) ameliorates myocardial ischemia-reperfusion injury and HF. Nuclear factor-erythroid-2-related factor 2 (Nrf2) regulates the antioxidant proteins expression and is upregulated by H2S. We examined the NaNO2 effects on endogenous H2S bioavailability and Nrf2 activation in mice subjected to ischemia-induced chronic heart failure (CHF). METHODS AND
resultsMice underwent 60 minutes of left coronary artery occlusion and 4 weeks of reperfusion. NaNO2 (165 μg/kgic) or vehicle was administered at reperfusion and then in drinking water (100 mg/L) for 4 weeks. Left ventricular (LV), ejection fraction (EF), LV end diastolic (LVEDD) and systolic dimensions (LVESD) were determined at baseline and at 4 weeks of reperfusion. Myocardial tissue was analyzed for oxidative stress and respective gene/protein-related assays. We found that NaNO2 therapy preserved LVEF, LVEDD and LVSD at 4 weeks during ischemia-induced HF. Myocardial malondialdehyde and protein carbonyl content were significantly reduced in NaNO2-treated mice as compared to vehicle, suggesting a reduction in oxidative stress. NaNO2 therapy markedly increased expression of Cu,Zn-superoxide dismutase, catalase, and glutathione peroxidase during 4 weeks of reperfusion. Furthermore, NaNO2 upregulated the activity of Nrf2, as well as H2S-producing enzymes, and ultimately increased H2S bioavailability in ischemia-induced CHF in mice as compared with vehicle.
conclusionsOur results demonstrate that NaNO2 therapy significantly improves LV function via increasing H2S bioavailability, Nrf2 activation, and antioxidant defenses.
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