ArticleArteriosclerosis, thrombosis, and vascular biology2013
Thioredoxin 1 is essential for sodium sulfide-mediated cardioprotection in the setting of heart failure.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 65 citations in OpenAlex.
- Hydrogen Sulfide Protects Erectile Function Through Stimulation of Antioxidant Defense in the Corpus Cavernosum: Insights From SG1002 Administration and Cystathionine γ-Lyase Knockout.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Role of Gut Microbial Metabolites in Ischemic and Non-Ischemic Heart Failure.International journal of molecular sciences · 2025Review
- Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.Biomolecules · 2024Review
- Review
- AP39 through AMPK-ULK1-FUNDC1 pathway regulates mitophagy, inhibits pyroptosis, and improves doxorubicin-induced myocardial fibrosis.iScience · 2024Article
- Receptor-dependent effects of sphingosine-1-phosphate (S1P) in COVID-19: the black side of the moon.Molecular and cellular biochemistry · 2023Article
- Cystathionine Gamma Lyase Is Regulated by Flow and Controls Smooth Muscle Migration in Human Saphenous Vein.Antioxidants (Basel, Switzerland) · 2023Article
- Mitochondrial Integrity Is Critical in Right Heart Failure Development.International journal of molecular sciences · 2023Review
- Clinical Potential of Hydrogen Sulfide in Peripheral Arterial Disease.International journal of molecular sciences · 2023Review
- Optimization of a Monobromobimane (MBB) Derivatization and RP-HPLC-FLD Detection Method for Sulfur Species Measurement in Human Serum after Sulfur Inhalation Treatment.Antioxidants (Basel, Switzerland) · 2022Article
- Clinical Use of Hydrogen Sulfide to Protect Against Intimal Hyperplasia.Frontiers in cardiovascular medicine · 2022Review
- A review of the effects of ticagrelor on adenosine concentration and its clinical significance.Pharmacological reports : PR · 2021Review
- Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021Article
- Genetically Encoded Fluorescent Redox Indicators for Unveiling Redox Signaling and Oxidative Toxicity.Chemical research in toxicology · 2021Review
- Txnip C247S mutation protects the heart against acute myocardial infarction.Journal of molecular and cellular cardiology · 2021Article
- Hydrogen Sulfide-Clues from Evolution and Implication for Neonatal Respiratory Diseases.Children (Basel, Switzerland) · 2021Review
- MZe786 Rescues Cardiac Mitochondrial Activity in High sFlt-1 and Low HO-1 Environment.Antioxidants (Basel, Switzerland) · 2020Article
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 2020Review
- Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson's Disease.International journal of molecular sciences · 2020Review
- Role of DJ-1 in Modulating Glycative Stress in Heart Failure.Journal of the American Heart Association · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThe aim of this study was to determine whether thioredoxin 1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure (HF). APPROACH AND
resultsMice with a cardiac-specific overexpression of a dominant negative mutant of Trx1 and wild-type littermates were subjected to ischemic-induced HF. Treatment with H2S as sodium sulfide (Na2S) not only increased the gene and protein expression of Trx1 in the absence of ischemia but also augmented the HF-induced increase in both. Wild-type mice treated with Na2S experienced less left-ventricular dilatation, improved left-ventricular function, and less cardiac hypertrophy after the induction of HF. In contrast, Na2S therapy failed to improve any of these parameters in the dominant negative mutant of Trx1 mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S therapy inhibited HF-induced apoptosis signaling kinase-1 signaling and nuclear export of histone deacetylase 4 in a Trx1-dependent manner.
conclusionsThese findings provide novel information that the upregulation of Trx1 by Na2S therapy in the setting of HF sets into motion events, such as the inhibition of apoptosis signaling kinase-1 signaling and histone deacetylase 4 nuclear export, which ultimately leads to the attenuationof left-ventricular remodeling.
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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.