ArticlePLoS genetics2016
Genetic Dissection of Cardiac Remodeling in an Isoproterenol-Induced Heart Failure Mouse Model.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 88 citations in OpenAlex.
- Article
- Integration of Collaborative Cross and Hybrid Mouse Diversity Panel studies does not significantly improve genome wide association study results.BMC research notes · 2026Article
- Genetic background is associated with distinct patterns of proarrhythmogenic remodeling leading to atrial fibrillation in pigs with ischemic heart failure.Basic research in cardiology · 2026Article
- Genetic determinants of heart failure susceptibility and response in the collaborative cross mouse population.Genetics · 2026Article
- Mapping DNA methylation to cardiac pathologies induced by beta-adrenergic stimulation in a large panel of mice.Epigenetics · 2025Article
- Novel insights into post-myocardial infarction cardiac remodeling through algorithmic detection of cell-type composition shifts.PLoS genetics · 2025Article
- Distinct morphometric features of cardiomyocytes isolated from mouse hypertrophy models: An ImageJ analysis combined with machine learning algorithms.Physiological reports · 2025Article
- Decoding the Liver-Heart Axis in Cardiometabolic Diseases.Circulation research · 2025Review
- Empagliflozin's cardioenergetic protective effects through PPARα pathway modulation in heart failure.Frontiers in pharmacology · 2025Article
- Heart failure induced by isoproterenol: A comparison of two doses and two delivery methods in C57BL/6J mice.PloS one · 2025Article
- NADPCurrent medicinal chemistry · 2025Review
- Rapid onset fibrotic remodeling and ventricular dysfunction induced by phenylephrine involve targeted reprogramming of myocyte and fibroblast transcriptomes.bioRxiv : the preprint server for biology · 2024Article
- Melatonin enhances captopril mediated cardioprotective effects and improves mitochondrial dynamics in male Wistar rats with chronic heart failure.Scientific reports · 2024Article
- Isoproterenol induced cardiac hypertrophy: A comparison of three doses and two delivery methods in C57BL/6J mice.PloS one · 2024Article
- Shexiang Tongxin Dropping Pill Allieviates Heart Failure via Extracellula Matrix-Receptor Interaction Pathways Based on RNA-Seq Transcriptomics and Experimental Studies.Chinese journal of integrative medicine · 2023Article
- Article
- Conserved multi-tissue transcriptomic adaptations to exercise training in humans and mice.Cell reports · 2023Article
- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Cardiomyocyte ploidy is dynamic during postnatal development and varies across genetic backgrounds.Development (Cambridge, England) · 2023Article
- Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
We aimed to understand the genetic control of cardiac remodeling using an isoproterenol-induced heart failure model in mice, which allowed control of confounding factors in an experimental setting. We characterized the changes in cardiac structure and function in response to chronic isoproterenol infusion using echocardiography in a panel of 104 inbred mouse strains. We showed that cardiac structure and function, whether under normal or stress conditions, has a strong genetic component, with heritability estimates of left ventricular mass between 61% and 81%. Association analyses of cardiac remodeling traits, corrected for population structure, body size and heart rate, revealed 17 genome-wide significant loci, including several loci containing previously implicated genes. Cardiac tissue gene expression profiling, expression quantitative trait loci, expression-phenotype correlation, and coding sequence variation analyses were performed to prioritize candidate genes and to generate hypotheses for downstream mechanistic studies. Using this approach, we have validated a novel gene, Myh14, as a negative regulator of ISO-induced left ventricular mass hypertrophy in an in vivo mouse model and demonstrated the up-regulation of immediate early gene Myc, fetal gene Nppb, and fibrosis gene Lgals3 in ISO-treated Myh14 deficient hearts compared to controls.
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.