ArticleJournal of the American Heart Association2020
Pressure Overload Greatly Promotes Neonatal Right Ventricular Cardiomyocyte Proliferation: A New Model for the Study of Heart Regeneration.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Right ventricular pressure overload disturbs T-tubule maturation via MEF2D's transcriptional regulation of BIN1.JCI insight · 2026Article
- A neonatal rat model of progressive left ventricular pressure overload induced by abdominal aortic banding microsurgery.JTCVS techniques · 2025Article
- Evaluation of Treatment Effect of Sirolimus on Pediatric Pulmonary Vein Stenosis Using a Neonatal Rat Model.JACC. Basic to translational science · 2025Article
- The unique hypertrophic and fibrotic features of neonatal right ventricle in response to pressure overload.Scientific reports · 2025Article
- Article
- Right ventricular volume overload reboots cardiomyocyte proliferation via immune responses.Journal of translational medicine · 2024Article
- Hemodynamic Melody of Postnatal Cardiac and Pulmonary Development in Children with Congenital Heart Diseases.Biology · 2024Review
- Effects and mechanisms of the myocardial microenvironment on cardiomyocyte proliferation and regeneration.Frontiers in cell and developmental biology · 2024Review
- Changes in glutamic oxaloacetic transaminase 2 during rat physiological and pathological cardiomyocyte hypertrophy.BMC cardiovascular disorders · 2023Article
- A neonatal rat model of pulmonary vein stenosis.Cell & bioscience · 2023Article
- Congenital heart disease-associated pulmonary dysplasia and its underlying mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Impaired cell-cell communication and axon guidance because of pulmonary hypoperfusion during postnatal alveolar development.Respiratory research · 2023Article
- Volume overload impedes the maturation of sarcomeres and T-tubules in the right atria: a potential cause of atrial arrhythmia following delayed atrial septal defect closure.Frontiers in physiology · 2023Article
- Ability of the Right Ventricle to Serve as a Systemic Ventricle in Response to the Volume Overload at the Neonatal Stage.Biology · 2022Article
- Article
- Molecular Changes in Prepubertal Left Ventricular Development Under Experimental Volume Overload.Frontiers in cardiovascular medicine · 2022Article
- Postnatal Right Ventricular Developmental Track Changed by Volume Overload.Journal of the American Heart Association · 2021Article
- Downregulated developmental processes in the postnatal right ventricle under the influence of a volume overload.Cell death discovery · 2021Article
- Volume Overload Initiates an Immune Response in the Right Ventricle at the Neonatal Stage.Frontiers in cardiovascular medicine · 2021Article
- A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Current mammalian models for heart regeneration research are limited to neonatal apex amputation and myocardial infarction, both of which are controversial. RNAseq has demonstrated a very limited set of differentially expressed genes between sham and operated hearts in myocardial infarction models. Here, we investigated in rats whether pressure overload in the right ventricle, a common phenomenon in children with congenital heart disease, could be used as a better animal model for heart regeneration studies when considering cardiomyocyte proliferation as the most important index. Methods and Results In the rat model, pressure overload was induced by pulmonary artery banding on postnatal day 1 and confirmed by echocardiography and hemodynamic measurements at postnatal day 7. RNA sequencing analyses of purified right ventricular cardiomyocytes at postnatal day 7 from pulmonary artery banding and sham-operated rats revealed that there were 5469 differentially expressed genes between these 2 groups. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis showed that these genes mainly mediated mitosis and cell division. Cell proliferation assays indicated a continuous overproliferation of cardiomyocytes in the right ventricle after pulmonary artery banding, in particular for the first 3 postnatal days. We also validated the model using samples from overloaded right ventricles of human patients. There was an approximately 2-fold increase of Ki67/pHH3/aurora B-positive cardiomyocytes in human-overloaded right ventricles compared with nonoverloaded right ventricles. Other features of this animal model included cardiomyocyte hypotrophy with no fibrosis. Conclusions Pressure overload profoundly promotes cardiomyocyte proliferation in the neonatal stage in both rats and human beings. This activates a regeneration-specific gene program and may offer an alternative animal model for heart regeneration research.
Indexed as
Identifiers
What OpenQuestion holds
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.