ArticleCirculation2025
Induced Cytokinesis Generates Highly Proliferative Mononuclear Cardiomyocytes at the Expense of Contractility.
Article in Circulation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dual-Target Cardiac Regeneration: ControllableCirculation · 2026Article
- Dynamic cardiac hyperplasia and hypertrophy in Burmese pythons.American journal of physiology. Cell physiology · 2026Article
- Epigenetic Control of Mammalian Cardiomyocyte Proliferation.Current cardiology reports · 2026Review
- The PIDDosome controls cardiomyocyte polyploidization during postnatal heart development.Cell death and differentiation · 2026Article
- Genes for 5'mRNA cap binding proteins, eif4ea and eif4eb, have alternative roles during heart regeneration.Developmental biology · 2026Article
- Ring canals in the larval adipose of Drosophila buffer stress response.The Journal of cell biology · 2026Article
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Authors and funding
19 authors.
Funding
Abstract
backgroundCytokinesis is the last step in the eukaryotic cell cycle, which physically separates a mitotic cell into 2 daughter cells. A few days after birth in mouse cardiomyocytes, DNA synthesis occurs without cytokinesis, leading to the majority of cardiomyocytes becoming binucleated instead of generating 2 daughter cells with 1 nucleus each. This results in cell cycle arrest of cardiomyocytes, and the mouse heart is no longer able to regenerate. A longstanding unanswered question is whether binucleation of cardiomyocytes is a result of cytokinesis failure.
methodsTo address this, we generated several transgenic mouse models to determine whether forced induction of cardiomyocyte cytokinesis generates mononucleated cardiomyocytes and restores the endogenous regenerative properties of the myocardium. We focused on 2 complementary regulators of cytokinesis: Plk1 (polo-like kinase 1) and Ect2 (epithelial cell-transformation sequence 2).
resultsWe found that cardiomyocyte-specific transgenic overexpression of constitutively active Plk1(T210D) promotes mitosis and cytokinesis in adult hearts, whereas overexpression of Ect2 alone promotes only cytokinesis. Cardiomyocyte-specific overexpression of both Plk1(T210D) and Ect2 concomitantly (double transgenic) prevents binucleation of cardiomyocytes postnatally and results in widespread cardiomyocyte mitosis, cardiac enlargement, contractile failure, and death before 2 weeks of age. In contrast, doxycycline-inducible cardiomyocyte-specific overexpression of both genes (inducible double transgenic) in the adult heart results in cardiomyocyte mitosis and transient contractile dysfunction. Importantly, this transient induction of cytokinesis in adult mice improves left ventricular systolic function after myocardial infarction.
conclusionsThese results collectively demonstrate that cytokinesis failure mediates cardiomyocyte multinucleation and cell cycle exit of postnatal cardiomyocytes, but may be a protective mechanism to preserve the contractile function of the myocardium.
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