ArticleJournal of the American Heart Association2015
Molecular Signature of Nitroso-Redox Balance in Idiopathic Dilated Cardiomyopathies.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- From amino-acid to disease: the effects of oxidation on actin-myosin interactions in muscle.Journal of muscle research and cell motility · 2023Review
- Nitrosative Stress and Human Disease: Therapeutic Potential of Denitrosylation.International journal of molecular sciences · 2021Review
- Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress.Antioxidants (Basel, Switzerland) · 2020Review
- Core functional nodes and sex-specific pathways in human ischaemic and dilated cardiomyopathy.Nature communications · 2020Article
- Human Relaxin-2 Fusion Protein Treatment Prevents and Reverses Isoproterenol-Induced Hypertrophy and Fibrosis in Mouse Heart.Journal of the American Heart Association · 2019Article
- A knock-in mutation at cysteine 144 of TRIM72 is cardioprotective and reduces myocardial TRIM72 release.Journal of molecular and cellular cardiology · 2019Article
- Integrated Dissection of Cysteine Oxidative Post-translational Modification Proteome During Cardiac Hypertrophy.Journal of proteome research · 2018Article
- The profile of selected single nucleotide polymorphisms in patients with hypertension and heart failure with preserved and mid-range ejection fraction.Scientific reports · 2017Article
- Sex Differences in Metabolic Cardiomyopathy.Cardiovascular research · 2017Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIdiopathic dilated cardiomyopathy is one of the most common types of cardiomyopathy. It has been proposed that an increase in oxidative stress in heart failure leads to a decrease in nitric oxide signaling, leading to impaired nitroso-redox signaling. To test this hypothesis, we investigated the occurrence of protein S-nitrosylation (SNO) and oxidation in biopsies from explanted dilated cardiomyopathy and nonfailing donor male and female human hearts. METHODS AND
resultsRedox-based resin-assisted capture for oxidation and SNO proteomic analysis was used to measure protein oxidation and SNO, respectively. In addition, 2-dimensional difference gel electrophoresis using maleimide sulfhydryl-reactive fluors was used to identify the SNO proteins. Protein oxidation increased in dilated cardiomyopathy biopsies in comparison with those from healthy donors. Interestingly, we did not find a consistent decrease in SNO in failing hearts; we found that some proteins showed an increase in SNO and others showed a decrease, and there were sex-specific differences in the response. We found 10 proteins with a significant decrease in SNO and 4 proteins with an increase in SNO in failing female hearts. Comparing nonfailing and failing male hearts, we found 9 proteins with a significant decrease and 12 proteins with a significant increase. We also found an increase in S-glutathionylation of endothelial nitric oxide synthase in failing female versus male hearts, suggesting an increase in uncoupled nitric oxide synthase in female hearts.
conclusionThese findings highlight the importance of nitroso-redox signaling in both physiological and pathological conditions, suggesting a potential target to treat heart failure.
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