ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Physiologic and molecular characterization of a murine model of right ventricular volume overload.
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 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Metabolic Remodeling in the Pressure-Loaded Right Ventricle: Shifts in Glucose and Fatty Acid Metabolism-A Systematic Review and Meta-Analysis.Journal of the American Heart Association · 2019Pooled it
- Long-Term Effects of Right Ventricular Pressure and Volume Overload: A Comparative Analysis in an Ovine Model.Journal of clinical medicine · 2026Article
- Right Heart Diastology, Where Are We Now?Circulation research · 2026Review
- Chronic therapy with α1A-adrenergic agonist reverses RV failure and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Impaired renal blood perfusion is closely related to right heart volume overload in congestive heart failure.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Article
- Right Heart Failure in Critical and Chronic Care: Current Concepts, Challenges and Mechanical Support Strategies.Medical sciences (Basel, Switzerland) · 2025Review
- Nonischemic Septal Fibrosis in Functional Tricuspid Regurgitation Provides Incremental Stratification of Adverse Remodeling and Prognosis.JACC. Cardiovascular imaging · 2025Article
- Dual inhibition of TGFβ and PDGF improves RV remodeling and function in response to RV pressure or volume-loading.Physiological reports · 2025Article
- Article
- Mouse Cardiovascular Imaging.Current protocols · 2024Review
- Disease severity, arrhythmogenesis, and fibrosis are related to longer action potentials in tetralogy of Fallot.Clinical research in cardiology : official journal of the German Cardiac Society · 2024Article
- A Noninvasive Circulating Signature of Combined Right Ventricular Pressure and Volume Overload in Tetralogy of Fallot/Pulmonary Atresia/Major Aortopulmonary Collateral Arteries.World journal for pediatric & congenital heart surgery · 2024Article
- Tetralogy of Fallot Across the Lifespan: A Focus on the Right Ventricle.CJC pediatric and congenital heart disease · 2023Review
- Characterizing the Spatiotemporal Transcriptomic Response of the Right Ventricle to Acute Pressure Overload.International journal of molecular sciences · 2023Article
- Transcriptome studies of congenital heart diseases: identifying current gaps and therapeutic frontiers.Frontiers in genetics · 2023Review
- The right ventricle in tetralogy of Fallot: adaptation to sequential loading.Frontiers in pediatrics · 2023Review
- Molecular signaling pathways in right ventricular impairment of adult patients after tetralogy of Fallot repair.Cardiovascular diagnosis and therapy · 2021Article
- Right ventricular phenotype, function, and failure: a journey from evolution to clinics.Heart failure reviews · 2021Review
- Right versus left ventricular remodeling in heart failure due to chronic volume overload.Scientific reports · 2021Article
- The role of mechanotransduction in heart failure pathobiology-a concise review.Heart failure reviews · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary insufficiency (PI) is a common long-term sequel after repair of tetralogy of Fallot, causing progressive right ventricular (RV) dilation and failure. We describe the physiologic and molecular characteristics of the first murine model of RV volume overload. PI was created by entrapping the pulmonary valve leaflets with sutures. Imaging, catheterization, and exercise testing were performed at 1, 3, and 6 mo and compared with sham controls. RNA from the RV free wall was hybridized to Agilent whole genome oligonucleotide microarrays. Volume overload resulted in RV enlargement, decreased RV outflow tract shortening fraction at 1 mo followed by normalization at 3 and 6 mo (39 ± 2, 44 ± 2, and 41 ± 2 vs. 46 ± 3% in sham), early reversal of early and late diastolic filling velocities (E/A ratio) followed by pseudonormalization (0.87 ± 0.08, 0.82 ± 0.08, and 0.96 ± 0.08 vs. 1.04 ± 0.03; P < 0.05), elevated end-diastolic pressure (7.6 ± 0.7, 6.9 ± 0.8, and 7 ± 0.5 vs. 2.7 ± 0.2 mmHg; P < 0.05), and decreased exercise duration (26 ± 0.4, 26 ± 1, and 22 ± 1.3 vs. 30 ± 1.1 min; P < 0.05). Subendocardial RV fibrosis was evident by 1 mo. At 1 mo, 372 genes were significantly downregulated. Mitochondrial pathways and G protein-coupled receptor signaling were the most represented categories. At 3 mo, 434 genes were upregulated and 307 downregulated. While many of the same pathways continued to be downregulated, TNF-α, transforming growth factor-β(1) (TGF-β(1)), p53-signaling, and extracellular matrix (ECM) remodeling transitioned from down- to upregulated. We describe a novel murine model of chronic RV volume overload recapitulating aspects of the clinical disease with gene expression changes suggesting early mitochondrial bioenergetic dysfunction, enhanced TGF-β signaling, ECM remodeling, and apoptosis.
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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.