ArticleJournal of the American Heart Association2021
Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload-Induced Right Ventricular Failure.
Article in Journal of the American Heart Association, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- A Cross-Species and Sex-Specific Meta-Analysis of Transcriptomic Studies of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2025Pooled it
- Human adult and pediatric multimodal transcriptomic atlas of progression from pressure-loaded to failing right ventricle.Nature cardiovascular research · 2026Article
- Beyond the Heart-Lung Axis: A Review of the Crosstalk Between the Hemodynamic, Neurohormonal, and Immune Systems in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- Mitochondrial electron transport chain is essential for acute inflammatory stress responses in mouse fibroblasts.Scientific reports · 2026Article
- From Oxidative Stress to Fibrotic Remodeling: Integrating Redox Biology, Galectin-3, and Imaging Phenotypes in Heart Failure.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- Chronic therapy with α1A-adrenergic agonist reverses RV failure and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Yixinjiedu Formula Attenuates Pressure Overload-Induced Cardiac Dysfunction by Suppressing Ferroptosis and Restoring Mitophagy via the PINK1/Parkin Axis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Gene Therapy for Heart Failure: Impact on Mitochondrial Dysfunction.Biomedicines · 2026Review
- Severe myocardium suppression in two congenital heart disease patients after remdesivir use - a case report.BMC pediatrics · 2025Article
- Adaptation to Elevated Mitochondrial Calcium Is Distinct in the Left and Right Ventricles.Circulation research · 2025Article
- Cellular and Transcriptional Landscape of Human Hypoplastic Left Heart Syndrome.Research square · 2025Article
- Optic Atrophy 1: The Conductor of Cellular Harmony and Age-Related Pathologies.Aging and disease · 2025Review
- Mitochondrial Dysfunction in Congenital Heart Disease.Journal of cardiovascular development and disease · 2025Review
- Mitochondria as a primary determinant of angiogenic modality in pulmonary arterial hypertension.The Journal of experimental medicine · 2024Article
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- Guidelines for mitochondrial RNA analysis.Molecular therapy. Nucleic acids · 2024Review
- Comparison of the stage-dependent mitochondrial changes in response to pressure overload between the diseased right and left ventricle in the rat.Basic research in cardiology · 2024Article
- Altered Inflammatory State and Mitochondrial Function Identified by Transcriptomics in Paediatric Congenital Heart Patients Prior to Surgical Repair.International journal of molecular sciences · 2024Article
- Pulmonary Hypertension and Right Ventricle: A Pathophysiological Insight.Clinical Medicine Insights. Cardiology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Background In complex congenital heart disease patients such as those with tetralogy of Fallot, the right ventricle (RV) is subject to pressure overload, leading to RV hypertrophy and eventually RV failure. The mechanisms that promote the transition from stable RV hypertrophy to RV failure are unknown. We evaluated the role of mitochondrial bioenergetics in the development of RV failure. Methods and Results We created a murine model of RV pressure overload by pulmonary artery banding and compared with sham-operated controls. Gene expression by RNA-sequencing, oxidative stress, mitochondrial respiration, dynamics, and structure were assessed in pressure overload-induced RV failure. RV failure was characterized by decreased expression of electron transport chain genes and mitochondrial antioxidant genes (aldehyde dehydrogenase 2 and superoxide dismutase 2) and increased expression of oxidant stress markers (heme oxygenase, 4-hydroxynonenal). The activities of all electron transport chain complexes decreased with RV hypertrophy and further with RV failure (oxidative phosphorylation: sham 552.3±43.07 versus RV hypertrophy 334.3±30.65 versus RV failure 165.4±36.72 pmol/(s×mL),
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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.