ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Reduction of cardiomyocyte S-nitrosylation by S-nitrosoglutathione reductase protects against sepsis-induced myocardial depression.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- S-Nitrosylation in Cardiovascular Disorders: The State of the Art.Biomolecules · 2025Review
- Ruxolitinib-based senomorphic therapy mitigates cardiomyocyte senescence in septic cardiomyopathy by inhibiting the JAK2/STAT3 signaling pathway.International journal of biological sciences · 2024Article
- Class III Alcohol Dehydrogenase Plays a Key Role in the Onset of Alcohol-Related/-Associated Liver Disease as an S-Nitrosoglutathione Reductase in Mice.International journal of molecular sciences · 2023Article
- Moderate exercise-induced dynamics on key sepsis-associated signaling pathways in the liver.Critical care (London, England) · 2023Article
- Cardiac Hypoxia Tolerance in Fish: From Functional Responses to Cell Signals.International journal of molecular sciences · 2023Review
- Cardiac-specific ITCH overexpression ameliorates septic cardiomyopathyJournal of molecular and cellular cardiology plus · 2022Article
- ADH5-mediated NO bioactivity maintains metabolic homeostasis in brown adipose tissue.Cell reports · 2021Article
- Hypoxic and Thermal Stress: Many Ways Leading to the NOS/NO System in the Fish Heart.Antioxidants (Basel, Switzerland) · 2021Review
- Long non-coding RNA GAS5 aggravates myocardial depression in mice with sepsis via the microRNA-449b/HMGB1 axis and the NF-κB signaling pathway.Bioscience reports · 2021Article
- Nitric Oxide and S-Nitrosylation in Cardiac Regulation: G Protein-Coupled Receptor Kinase-2 and β-Arrestins as Targets.International journal of molecular sciences · 2021Review
- An Overview of Investigational and Experimental Drug Treatment Strategies for Marfan Syndrome.Journal of experimental pharmacology · 2021Review
- Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress.Antioxidants (Basel, Switzerland) · 2020Review
- Shank3 mutation in a mouse model of autism leads to changes in the S-nitroso-proteome and affects key proteins involved in vesicle release and synaptic function.Molecular psychiatry · 2020Article
- The Hypoxia Tolerance of the Goldfish (Antioxidants (Basel, Switzerland) · 2020Article
- An emerging perspective on sex differences: Intersecting S-nitrosothiol and aldehyde signaling in the heart.Redox biology · 2020Review
- nNOS/GSNOR interaction contributes to skeletal muscle differentiation and homeostasis.Cell death & disease · 2019Article
- Protein S-Nitrosylation: Determinants of Specificity and Enzymatic Regulation of S-Nitrosothiol-Based Signaling.Antioxidants & redox signaling · 2019Review
- Improvement in Outcomes After Cardiac Arrest and Resuscitation by Inhibition of S-Nitrosoglutathione Reductase.Circulation · 2019Article
- S-Nitrosoglutathione Reductase Is Essential for Protecting the Female Heart From Ischemia-Reperfusion Injury.Circulation research · 2018Article
- Nitrosative Stress, Hypernitrosylation, and Autoimmune Responses to Nitrosylated Proteins: New Pathways in Neuroprogressive Disorders Including Depression and Chronic Fatigue Syndrome.Molecular neurobiology · 2017Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Myocardial depression is an important contributor to morbidity and mortality in septic patients. Nitric oxide (NO) plays an important role in the development of septic cardiomyopathy, but also has protective effects. Recent evidence has indicated that NO exerts many of its downstream effects on the cardiovascular system via protein S-nitrosylation, which is negatively regulated by S-nitrosoglutathione reductase (GSNOR), an enzyme promoting denitrosylation. We tested the hypothesis that reducing cardiomyocyte S-nitrosylation by increasing GSNOR activity can improve myocardial dysfunction during sepsis. Therefore, we generated mice with a cardiomyocyte-specific overexpression of GSNOR (GSNOR-CMTg mice) and subjected them to endotoxic shock. Measurements of cardiac function in vivo and ex vivo showed that GSNOR-CMTg mice had a significantly improved cardiac function after lipopolysaccharide challenge (LPS, 50 mg/kg) compared with wild-type (WT) mice. Cardiomyocytes isolated from septic GSNOR-CMTg mice showed a corresponding improvement in contractility compared with WT cells. However, systolic Ca(2+) release was similarly depressed in both genotypes after LPS, indicating that GSNOR-CMTg cardiomyocytes have increased Ca(2+) sensitivity during sepsis. Parameters of inflammation were equally increased in LPS-treated hearts of both genotypes, and no compensatory changes in NO synthase expression levels were found in GSNOR-overexpressing hearts before or after LPS challenge. GSNOR overexpression however significantly reduced total cardiac protein S-nitrosylation during sepsis. Taken together, our results indicate that increasing the denitrosylation capacity of cardiomyocytes protects against sepsis-induced myocardial depression. Our findings suggest that specifically reducing protein S-nitrosylation during sepsis improves cardiac function by increasing cardiac myofilament sensitivity to Ca(2+).
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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.