ArticleCirculation research2022
Mitochondrial H
Article in Circulation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Article
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Commentary: Unveiling a Metabolic-Lymphatic Axis in the Pathogenesis of Heart Failure With Preserved Ejection Fraction.Cardiology discovery · 2026Article
- Diet-Associated Regulation of Cardiac Metabolism: Molecular Determinants and Pathophysiological Consequences.Nutrients · 2026Review
- BCAA Metabolic Dyshomeostasis in Cardiovascular Disease: Pathogenic Mechanisms and Intervention.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026Review
- Quantitative proteomics links mitochondrial dysfunction to metabolic changes and epithelial differentiation defects in hyperoxia-exposed neonatal airway cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Research progress on metabolic abnormalities in myocardial hypertrophy.Frontiers in cardiovascular medicine · 2026Review
- A Serinol-Modified 1,8-Naphthalimide Fluorescent Probe for Selective Detection of H₂S in Human Serum and Hypertensive Patients.Journal of fluorescence · 2026Article
- Cardiovascular Disease Meets Cancer: Exploring the Epidemiology in China and Homotherapy Targeting Intersectional Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Hydrogen Sulfide Deficiency and Therapeutic Targeting in Cardiometabolic HFpEF: Evidence for Synergistic Benefit With GLP-1/Glucagon Agonism.JACC. Basic to translational science · 2025Article
- Branched-Chain α Keto-Acid Dehydrogenase Kinase-Mediated AKT Phosphorylation Promotes RCC Tumorigenesis and Drug Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Low Dose GLP-1 Therapy Attenuates Pathological Cardiac and Hepatic Remodelling in HFpEF Independent of Weight Loss.bioRxiv : the preprint server for biology · 2025Article
- Relationship between amino acid metabolism and inflammation in coronary heart disease (Review).International journal of molecular medicine · 2025Review
- Emerging Insights into the Relationship Between Amino Acid Metabolism and Diabetic Cardiomyopathy.Biomolecules · 2025Review
- Role of 3-mercaptopyruvate sulfurtransferase in cancer: Molecular mechanisms and therapeutic perspectives.Translational oncology · 2025Review
- BCAA catabolism targeted therapy for heart failure with preserved ejection fraction.Theranostics · 2025Article
- Alcohol-induced gut microbial reorganization and associated overproduction of phenylacetylglutamine promotes cardiovascular disease.Nature communications · 2024Article
- Adjunctive therapy with an oral HBritish journal of pharmacology · 2024Article
- Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.Biomolecules · 2024Review
- HProceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundHydrogen sulfide (H
methodsHuman myocardial samples obtained from patients with heart failure undergoing cardiac surgeries were probed for 3-MST protein expression. 3-MST knockout mice and C57BL/6J wild-type mice were subjected to transverse aortic constriction to induce pressure overload heart failure with reduced ejection fraction. Cardiac structure and function, vascular reactivity, exercise performance, mitochondrial respiration, and ATP synthesis efficiency were assessed. In addition, untargeted metabolomics were utilized to identify key pathways altered by 3-MST deficiency.
resultsMyocardial 3-MST was significantly reduced in patients with heart failure compared with nonfailing controls. 3-MST KO mice exhibited increased accumulation of branched-chain amino acids in the myocardium, which was associated with reduced mitochondrial respiration and ATP synthesis, exacerbated cardiac and vascular dysfunction, and worsened exercise performance following transverse aortic constriction. Restoring myocardial branched-chain amino acid catabolism with 3,6-dichlorobenzo1[b]thiophene-2-carboxylic acid (BT2) and administration of a potent H
conclusionsOur data suggest that 3-MST derived mitochondrial H
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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 Socratic graph.