ArticleProceedings of the National Academy of Sciences of the United States of America2015
Cardiac myosin binding protein C regulates postnatal myocyte cytokinesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- Early fibrotic gene activation precedes structural remodeling in the heart of cardiac myosin binding protein-C knockout mice.Physiological genomics · 2026Article
- Perinatal death in pig models of hypertrophic cardiomyopathy carrying sarcomere pathogenic variants.Journal of molecular and cellular cardiology plus · 2025Article
- Integrated single-cell functional-proteomic profiling reveals a shift in myofibre specificity in human nemaline myopathy: A proof-of-principle study.The Journal of physiology · 2025Article
- Myocardial dysfunction caused by MyBPC3 P459fs mutation in hypertrophic cardiomyopathy: evidence from multi-omics approaches and super-resolution imaging.Frontiers in cardiovascular medicine · 2025Article
- A New Ex Vivo Model to Study Cardiac Fibrosis in Whole Mouse Hearts.JACC. Basic to translational science · 2024Article
- MicroRNA205: A Key Regulator of Cardiomyocyte Transition from Proliferative to Hypertrophic Growth in the Neonatal Heart.International journal of molecular sciences · 2024Article
- Detection of PatIent-Level distances from single cell genomics and pathomics data with Optimal Transport (PILOT).Molecular systems biology · 2024Article
- Review
- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
- Transcriptome Profile Identifies Actin as an Essential Regulator of Cardiac Myosin Binding Protein C3 Hypertrophic Cardiomyopathy in a Zebrafish Model.International journal of molecular sciences · 2022Article
- Article
- Transient Cell Cycle Induction in Cardiomyocytes to Treat Subacute Ischemic Heart Failure.Circulation · 2022Article
- Live cell screening identifies glycosides as enhancers of cardiomyocyte cell cycle activity.Frontiers in cardiovascular medicine · 2022Article
- Long-term culture of patient-derived cardiac organoids recapitulated Duchenne muscular dystrophy cardiomyopathy and disease progression.Frontiers in cell and developmental biology · 2022Article
- Heterogeneous Distribution of Genetic Mutations in Myosin Binding Protein-C Paralogs.Frontiers in genetics · 2022Article
- Cardiomyocyte Proliferative Capacity Is Restricted in Mice WithFrontiers in cardiovascular medicine · 2021Article
- Modulation of SERCA2a expression and function by ultrasound-guided myocardial gene transfection.Experimental and therapeutic medicine · 2020Article
- Vagus nerve stimulation optimized cardiomyocyte phenotype, sarcomere organization and energy metabolism in infarcted heart through FoxO3A-VEGF signaling.Cell death & disease · 2020Article
- Age-Related Pathways in Cardiac Regeneration: A Role for lncRNAs?Frontiers in physiology · 2020Review
- Upregulation of Yy1 Suppresses Dilated Cardiomyopathy caused by Ttn insufficiency.Scientific reports · 2019Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Homozygous cardiac myosin binding protein C-deficient (Mybpc(t/t)) mice develop dramatic cardiac dilation shortly after birth; heart size increases almost twofold. We have investigated the mechanism of cardiac enlargement in these hearts. Throughout embryogenesis myocytes undergo cell division while maintaining the capacity to pump blood by rapidly disassembling and reforming myofibrillar components of the sarcomere throughout cell cycle progression. Shortly after birth, myocyte cell division ceases. Cardiac MYBPC is a thick filament protein that regulates sarcomere organization and rigidity. We demonstrate that many Mybpc(t/t) myocytes undergo an additional round of cell division within 10 d postbirth compared with their wild-type counterparts, leading to increased numbers of mononuclear myocytes. Short-hairpin RNA knockdown of Mybpc3 mRNA in wild-type mice similarly extended the postnatal window of myocyte proliferation. However, adult Mybpc(t/t) myocytes are unable to fully regenerate the myocardium after injury. MYBPC has unexpected inhibitory functions during postnatal myocyte cytokinesis and cell cycle progression. We suggest that human patients with homozygous MYBPC3-null mutations develop dilated cardiomyopathy, coupled with myocyte hyperplasia (increased cell number), as observed in Mybpc(t/t) mice. Human patients, with heterozygous truncating MYBPC3 mutations, like mice with similar mutations, have hypertrophic cardiomyopathy. However, the mechanism leading to hypertrophic cardiomyopathy in heterozygous MYBPC3(+/-) individuals is myocyte hypertrophy (increased cell size), whereas the mechanism leading to cardiac dilation in homozygous Mybpc3(-/-) mice is primarily myocyte hyperplasia.
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