ArticleThe Journal of biological chemistry2014
Repression of cyclin D1 expression is necessary for the maintenance of cell cycle exit in adult mammalian cardiomyocytes.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
- Epigenetic Control of Mammalian Cardiomyocyte Proliferation.Current cardiology reports · 2026Review
- Review
- Benzyl isothiocyanate induces heart regeneration.iScience · 2025Article
- Cell Reprogramming, Transdifferentiation, and Dedifferentiation Approaches for Heart Repair.International journal of molecular sciences · 2025Review
- Recent Insights into Endogenous Mammalian Cardiac Regeneration Post-Myocardial Infarction.International journal of molecular sciences · 2024Review
- Targeting cardiomyocyte cell cycle regulation in heart failure.Basic research in cardiology · 2024Review
- Regulation of endogenous cardiomyocyte proliferation: The known unknowns.Journal of molecular and cellular cardiology · 2023Review
- Metabolic Determinants in Cardiomyocyte Function and Heart Regenerative Strategies.Metabolites · 2022Review
- Apoptosis-associated speck-like protein containing a CARD regulates the growth of pancreatic ductal adenocarcinoma.Scientific reports · 2021Article
- Cardiomyocyte Proliferation as a Source of New Myocyte Development in the Adult Heart.International journal of molecular sciences · 2021Review
- Induced Cardiomyocyte Proliferation: A Promising Approach to Cure Heart Failure.International journal of molecular sciences · 2021Review
- Evidence that the acetyltransferase Tip60 induces the DNA damage response and cell-cycle arrest in neonatal cardiomyocytes.Journal of molecular and cellular cardiology · 2021Article
- Article
- microRNA-1 inhibits cardiomyocyte proliferation in mouse neonatal hearts by repressing CCND1 expression.Annals of translational medicine · 2019Article
- Intrauterine Programming of Diabetes Induced Cardiac Embryopathy.Diabetes & obesity international journal · 2019Article
- Silencing or not silencingJournal of thoracic disease · 2018Article
- A zebrafish model of infection-associated acute kidney injury.American journal of physiology. Renal physiology · 2018Article
- Polyploidy in tissue homeostasis and regeneration.Development (Cambridge, England) · 2018Review
- Cardiomyocyte Proliferation for Therapeutic Regeneration.Current cardiology reports · 2018Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hearts of neonatal mice and adult zebrafish can regenerate after injury through proliferation of preexisting cardiomyocytes. However, adult mammals are not capable of cardiac regeneration because almost all cardiomyocytes exit their cell cycle. Exactly how the cell cycle exit is maintained and how many adult cardiomyocytes have the potential to reenter the cell cycle are unknown. The expression and activation levels of main cyclin-cyclin-dependent kinase (CDK) complexes are extremely low or undetectable at adult stages. The nuclear DNA content of almost all cardiomyocytes is 2C, indicating the cell cycle exit from G1-phase. Here, we induced expression of cyclin D1, which regulates the progression of G1-phase, only in differentiated cardiomyocytes of adult mice. In these cardiomyocytes, S-phase marker-positive cardiomyocytes and the expression of main cyclins and CDKs increased remarkably, although cyclin B1-CDK1 activation was inhibited in an ATM/ATR-independent manner. The phosphorylation pattern of CDK1 and expression pattern of Cdc25 subtypes suggested that a deficiency in the increase in Cdc25 (a and -b), which is required for M-phase entry, inhibited the cyclin B1-CDK1 activation. Finally, analysis of cell cycle distribution patterns showed that >40% of adult mouse cardiomyocytes reentered the cell cycle by the induction of cyclin D1. The cell cycle of these binucleated cardiomyocytes was arrested before M-phase, and many mononucleated cardiomyocytes entered endoreplication. These data indicate that silencing the cyclin D1 expression is necessary for the maintenance of the cell cycle exit and suggest a mechanism that involves inhibition of M-phase entry.
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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.