ArticleCell proliferation2008
Phosphorylation of pRb by cyclin D kinase is necessary for development of cardiac hypertrophy.
Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Revitalizing the heart: strategies and tools for cardiomyocyte regeneration post-myocardial infarction.NPJ Regenerative medicine · 2025Review
- Ploidy-stratified single cardiomyocyte transcriptomics map Zinc Finger E-Box Binding Homeobox 1 to underly cardiomyocyte proliferation before birth.Basic research in cardiology · 2023Article
- Article
- Reawakening the Intrinsic Cardiac Regenerative Potential: Molecular Strategies to Boost Dedifferentiation and Proliferation of Endogenous Cardiomyocytes.Frontiers in cardiovascular medicine · 2021Review
- Effect of Triptolide on Temporal Expression of Cell Cycle Regulators During Cardiac Hypertrophy.Frontiers in pharmacology · 2020Article
- MicroRNAs in Cardiac Hypertrophy.International journal of molecular sciences · 2019Review
- Adaptation of Human iPSC-Derived Cardiomyocytes to Tyrosine Kinase Inhibitors Reduces Acute Cardiotoxicity via Metabolic Reprogramming.Cell systems · 2019Article
- Understanding cardiomyocyte proliferation: an insight into cell cycle activity.Cellular and molecular life sciences : CMLS · 2017Review
- CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy.Molecular and cellular biochemistry · 2016Article
- Attenuation of microRNA-16 derepresses the cyclins D1, D2 and E1 to provoke cardiomyocyte hypertrophy.Journal of cellular and molecular medicine · 2015Article
- Micro-RNA expression in hypoplastic left heart syndrome.Journal of cardiac failure · 2015Article
- Expressions and clinical significances of c-MET, p-MET and E2f-1 in human gastric carcinoma.BMC research notes · 2014Article
- Propranolol enhances cell cycle-related gene expression in pressure overloaded hearts.British journal of pharmacology · 2011Article
- Myocyte proliferation in the developing heart.Developmental dynamics : an official publication of the American Association of Anatomists · 2011Review
- Knockdown of cyclin-dependent kinase inhibitors induces cardiomyocyte re-entry in the cell cycle.The Journal of biological chemistry · 2011Article
- Sp1 phosphorylation and its regulation of gene transcription.Molecular and cellular biology · 2009Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesA number of stimuli induce cardiac hypertrophy and may lead to cardiomyopathy and heart failure. It is believed that cardiomyocytes withdraw from the cell cycle shortly after birth and become terminally differentiated. However, cell cycle regulatory proteins take part in the development of hypertrophy, and it is important to elucidate the mechanisms of how these proteins are involved in the hypertrophic response in cardiomyocytes. MATERIALS AND METHODS, AND
resultsIn the present study, by immunohistochemistry with a phosphorylation-specific antibody, we found that cyclin D-cdk4/6-phosphorylated retinoblastoma protein (pRb) during hypertrophy and expression of an unphosphorylatable pRb mutant impaired hypertrophic growth in cardiomyocytes. Transcription factor E2F was activated by hypertrophic elicitors but activation was impaired by pharmacological inhibition of cyclin D-cdk4/6. Inhibition of cyclin E-cdk2 complex only partly impaired E2F activity and did not prevent hypertrophic growth, but diminished endoreplication during hypertrophy.
conclusionsThese results indicate that cyclin D-cdk4/6-dependent phosphorylation of pRb and activation of E2F is necessary for hypertrophic growth in cardiomyocytes, whereas cyclin E-cdk2 kinase is not necessary for hypertrophy but regulates endoreplication in these cells. The data support the notion that hypertrophic growth of cardiomyocytes involves a partial progression through the G1 phase of the cell cycle
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