ArticleScientific reports2019
Re-enforcing hypoxia-induced polyploid cardiomyocytes enter cytokinesis through activation of β-catenin.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Article
- Dynamic map illuminates Hippo-cMyc module crosstalk driving cardiomyocyte proliferation.Development (Cambridge, England) · 2025Article
- Targeting cardiomyocyte cell cycle regulation in heart failure.Basic research in cardiology · 2024Review
- Drug-resilient Cancer Cell Phenotype Is Acquired via Polyploidization Associated with Early Stress Response Coupled to HIF2α Transcriptional Regulation.Cancer research communications · 2024Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Proliferation and Maturation: Janus and the Art of Cardiac Tissue Engineering.Circulation research · 2023Review
- Single-cell transcriptomics reveal extracellular vesicles secretion with a cardiomyocyte proteostasis signature during pathological remodeling.Communications biology · 2023Article
- The effects of β-catenin on cardiomyogenesis via Islet-1 and MLIP ubiquitination.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Polyploidy in Tissue Repair and Regeneration.Cold Spring Harbor perspectives in biology · 2021Review
- Endocrine Influence on Cardiac Metabolism in Development and Regeneration.Endocrinology · 2021Review
- Cardiomyocyte cell cycling, maturation, and growth by multinucleation in postnatal swine.Journal of molecular and cellular cardiology · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocyte (CM) loss is a characteristic of various heart diseases, including ischaemic heart disease. Cardiac regeneration has been suggested as a promising strategy to address CM loss. Although many studies of regeneration have focused mainly on mononucleated or diploid CM, the limitations associated with the cytokinesis of polyploid and multinucleated CMs remain less well known. Here, we show that β-catenin, a key regulator in heart development, can increase cytokinesis in polyploid multinucleated CMs. The activation of β-catenin increases the expression of the cytokinesis-related factor epithelial cell transforming 2 (ECT2), which regulates the actomyosin ring and thus leads to the completion of cytokinesis in polyploid CMs. In addition, hypoxia can induce polyploid and multinucleated CMs by increasing factors related to the G1-S-anaphase of the cell cycle, but not those related to cytokinesis. Our study therefore reveals that the β-catenin can promote the cytokinesis of polyploid multinucleated CMs via upregulation of ECT2. These findings suggest a potential field of polyploid CM research that may be exploitable for cardiac regeneration therapy.
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