ArticlePloS one2013
Biventricular remodeling in murine models of right ventricular pressure overload.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Left ventricular pressure-loading improves pressure-induced right ventricular remodeling by redistributing mechanical load and reducing mechanosignaling.Physiological reports · 2025Article
- Simultaneous Positron Emission Tomography and Molecular Magnetic Resonance Imaging of Cardiopulmonary Fibrosis in a Mouse Model of Left Ventricular Dysfunction.Journal of the American Heart Association · 2024Article
- A Comprehensive Review of Dilated Cardiomyopathy in Pre-clinical Animal Models in Addition to Herbal Treatment Options and Multi-modality Imaging Strategies.Cardiovascular & hematological disorders drug targets · 2023Review
- Glycolysis regulated transglutaminase 2 activation in cardiopulmonary fibrogenic remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Small animal models of heart failure.Cardiovascular research · 2019Review
- Bone Morphogenetic Protein 9 Reduces Cardiac Fibrosis and Improves Cardiac Function in Heart Failure.Circulation · 2018Article
- Fibroblasts and the extracellular matrix in right ventricular disease.Cardiovascular research · 2017Review
- Conditional knockout of activin like kinase-1 (ALK-1) leads to heart failure without maladaptive remodeling.Heart and vessels · 2017Article
- Pressure overload leads to an increased accumulation and activity of mast cells in the right ventricle.Physiological reports · 2017Article
- Reducing endoglin activity limits calcineurin and TRPC-6 expression and improves survival in a mouse model of right ventricular pressure overload.Journal of the American Heart Association · 2014Article
- Triggering the succinate receptor GPR91 enhances pressure overload-induced right ventricular hypertrophy.International journal of clinical and experimental pathology · 2014Article
- Reduced activin receptor-like kinase 1 activity promotes cardiac fibrosis in heart failure.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
- Pressure overload induced right ventricular remodeling is not attenuated by the anti-fibrotic agent pirfenidone.Pulmonary circulationArticle
- Management of Post-Myocardial Infarction Right Ventricular Failure.Journal of the Society for Cardiovascular Angiography & InterventionsReview
- Endoglin selectively modulates transient receptor potential channel expression in left and right heart failure.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledRight ventricular (RV) failure is a major cause of mortality in acute or chronic lung disease and left heart failure. The objective of this study was to demonstrate a percutaneous approach to study biventricular hemodynamics in murine models of primary and secondary RV pressure overload (RVPO) and further explore biventricular expression of two key proteins that regulate cardiac remodeling: calcineurin and transforming growth factor beta 1 (TGFβ1).
methodsAdult, male mice underwent constriction of the pulmonary artery or thoracic aorta as models of primary and secondary RVPO, respectively. Conductance catheterization was performed followed by tissue analysis for changes in myocyte hypertrophy and fibrosis.
resultsBoth primary and secondary RVPO decreased biventricular stroke work however RV instantaneous peak pressure (dP/dtmax) and end-systolic elastance (Ees) were preserved in both groups compared to controls. In contrast, left ventricular (LV) dP/dtmax and LV-Ees were unchanged by primary, but reduced in the secondary RVPO group. The ratio of RV:LV ventriculo-arterial coupling was increased in primary and reduced in secondary RVPO. Primary and secondary RVPO increased RV mass, while LV mass decreased in primary and increased in the secondary RVPO groups. RV fibrosis and hypertrophy were increased in both groups, while LV fibrosis and hypertrophy were increased in secondary RVPO only. RV calcineurin expression was increased in both groups, while LV expression increased in secondary RVPO only. Biventricular TGFβ1 expression was increased in both groups.
conclusionThese data identify distinct effects of primary and secondary RVPO on biventricular structure, function, and expression of key remodeling pathways.
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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.