ArticleThe EMBO journal2006
Hypertrophic growth in cardiac myocytes is mediated by Myc through a Cyclin D2-dependent pathway.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Meta-analysis of expression signatures of muscle atrophy: gene interaction networks in early and late stages.BMC genomics · 2008Pooled it
- Hypoxia-driven microRNA-27b underlies pathologic cardiac endoreplication in heart disease.Signal transduction and targeted therapy · 2026Article
- Article
- Protein O-GlcNAcylation in Health and Diseases.MedComm · 2025Review
- Targeting Cardiomyocyte PCNA and POLD1 Prevents Pathologic Myocardial Hypertrophy.Circulation research · 2025Article
- Myc overexpression improves recovery from myocardial infarction associated with cardiomyocyte hyperplasia in the mouse heart.Communications biology · 2025Article
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- Muscle fiber Myc is dispensable for muscle growth and its forced expression severely perturbs homeostasis.Nature communications · 2025Article
- Lnc PVT1 facilitates TGF-β1-induced human cardiac fibroblast activation in vitro and ISO-induced myocardial fibrosis in vivo through regulating MYC.Molecular and cellular biochemistry · 2025Article
- CCND2 Modified mRNA Activates Cell Cycle of Cardiomyocytes in Hearts With Myocardial Infarction in Mice and Pigs.Circulation research · 2023Article
- STAT5b is a key effector of NRG-1/ERBB4-mediated myocardial growth.EMBO reports · 2023Article
- Mitochondrial Creatine Kinase Attenuates Pathologic Remodeling in Heart Failure.Circulation research · 2022Observational
- Multi-Omics Characterization of a Human Stem Cell-Based Model of Cardiac Hypertrophy.Life (Basel, Switzerland) · 2022Article
- KSHV transactivator-derived small peptide traps coactivators to attenuate MYC and inhibits leukemia and lymphoma cell growth.Communications biology · 2021Article
- Role ofPhysiological reviews · 2021Review
- Lnc-GD2H Promotes Proliferation by Forming a Feedback Loop With c-Myc and Enhances Differentiation Through Interacting With NACA to Upregulate Myog in C2C12 Myoblasts.Frontiers in cell and developmental biology · 2021Article
- Investigating the Potential for Ultraviolet Light to Modulate Morbidity and Mortality From COVID-19: A Narrative Review and Update.Frontiers in cardiovascular medicine · 2020Review
- Upregulation of Yy1 Suppresses Dilated Cardiomyopathy caused by Ttn insufficiency.Scientific reports · 2019Article
- Repressive histone methylation regulates cardiac myocyte cell cycle exit.Journal of molecular and cellular cardiology · 2018Article
- AMPK activation counteracts cardiac hypertrophy by reducing O-GlcNAcylation.Nature communications · 2018Article
4 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 2 institutions in 2 countries.
Funding
Abstract
c-Myc (Myc) is highly expressed in developing embryos where it regulates body size by controlling proliferation but not cell size. However, Myc is also induced in many postmitotic tissues, including adult myocardium, in response to stress where the predominant form of growth is an increase in cell size (hypertrophy) and not number. The function of Myc induction in this setting is unproven. Therefore, to explore Myc's role in hypertrophic growth, we created mice where Myc can be inducibly inactivated, specifically in adult myocardium. Myc-deficient hearts demonstrated attenuated stress-induced hypertrophic growth, secondary to a reduction in cell growth of individual myocytes. To explore the dependence of Myc-induced cell growth on CycD2, we created bigenic mice where Myc can be selectively activated in CycD2-null adult myocardium. Myc-dependent hypertrophic growth and cell cycle reentry is blocked in CycD2-deficient hearts. However, in contrast to Myc-induced DNA synthesis, hypertrophic growth is independent of CycD2-induced Cdk2 activity. These data suggest that Myc is required for a normal hypertrophic response and that its growth-promoting effects are also mediated through a CycD2-dependent pathway.
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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.