ArticleJournal of the American Heart Association2013
Inactivation of Myosin binding protein C homolog in zebrafish as a model for human cardiac hypertrophy and diastolic dysfunction.
Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Zebrafish in Cardiovascular Disease Research: from Model to Application.International journal of biological sciences · 2026Review
- Orthologs at the Base of the Olfactores Clade.Genes · 2024Review
- Forward genetic screen using a gene-breaking trap approach identifies a novel role ofFrontiers in cell and developmental biology · 2024Article
- RBPMS2 Is a Myocardial-Enriched Splicing Regulator Required for Cardiac Function.Circulation research · 2022Article
- Genotype-Phenotype Associations with Restrictive Cardiomyopathy Induced by Pathogenic Genetic Mutations.Reviews in cardiovascular medicine · 2022Review
- Study on diverse pathological characteristics of heart failure in different stages based on proteomics.Journal of cellular and molecular medicine · 2022Article
- Transcriptome-Based Identification of Genes Responding to the Organophosphate Pesticide Phosmet inGenes · 2021Article
- Zebrafish Heart Failure Models.Frontiers in cell and developmental biology · 2021Review
- Cardiomyopathy with lethal arrhythmias associated with inactivation of KLHL24.Human molecular genetics · 2019Article
- Allelic imbalance and haploinsufficiency in MYBPC3-linked hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Knockdown of fast skeletal myosin-binding protein C in zebrafish results in a severe skeletal myopathy.The Journal of general physiology · 2016Article
- Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation.Nature communications · 2016Article
- Early-life perturbations in glucocorticoid activity impacts on the structure, function and molecular composition of the adult zebrafish (Danio rerio) heart.Molecular and cellular endocrinology · 2015Article
- Cross-tissue and cross-species analysis of gene expression in skeletal muscle and electric organ of African weakly-electric fish (Teleostei; Mormyridae).BMC genomics · 2015Article
- Novel Phenotype-Genotype Correlations of Restrictive Cardiomyopathy With Myosin-Binding Protein C (MYBPC3) Gene Mutations Tested by Next-Generation Sequencing.Journal of the American Heart Association · 2015Article
- Hook, line and sinker: adult zebrafish offer a valid model to study mammalian cardiac contractile mechanics.The Journal of physiology · 2014Article
- Understanding cardiac sarcomere assembly with zebrafish genetics.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSudden cardiac death due to malignant ventricular arrhythmia is a devastating manifestation of cardiac hypertrophy. Sarcomere protein myosin binding protein C is functionally related to cardiac diastolic function and hypertrophy. Zebrafish is a better model to study human electrophysiology and arrhythmia than rodents because of the electrophysiological characteristics similar to those of humans. METHODS AND
resultsWe established a zebrafish model of cardiac hypertrophy and diastolic dysfunction by genetic knockdown of myosin binding protein C gene (mybpc3) and investigated the electrophysiological phenotypes in this model. We found expression of zebrafish mybpc3 restrictively in the heart and slow muscle, and mybpc3 gene was evolutionally conservative with sequence homology between zebrafish and human mybpc3 genes. Zebrafish with genetic knockdown of mybpc3 by morpholino showed ventricular hypertrophy with increased myocardial wall thickness and diastolic heart failure, manifesting as decreased ventricular diastolic relaxation velocity, pericardial effusion, and dilatation of the atrium. In terms of electrophysiological phenotypes, mybpc3 knockdown fish had a longer ventricular action potential duration and slower ventricular diastolic calcium reuptake, both of which are typical electrophysiological features in human cardiac hypertrophy and heart failure. Impaired calcium reuptake resulted in increased susceptibility to calcium transient alternans and action potential duration alternans, which have been proved to be central to the genesis of malignant ventricular fibrillation and a sensitive marker of sudden cardiac death.
conclusionsmybpc3 knockdown in zebrafish recapitulated the morphological, mechanical, and electrophysiological phenotypes of human cardiac hypertrophy and diastolic heart failure. Our study also first demonstrated arrhythmogenic cardiac alternans in cardiac hypertrophy.
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