ArticlePloS one2018
Ezh2 is not required for cardiac regeneration in neonatal mice.
Article in PloS one, 2018. 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, 21 citations in OpenAlex.
- Molecular and Chromatin Accessibility Programs Underlying Epithelial Injury and Impaired Regeneration in Neonatal Necrotizing Enterocolitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Review
- Systematic genetic perturbation reveals principles underpinning robustness of the epigenetic regulatory network.Nucleic acids research · 2025Article
- Visualization of regenerating and repairing hearts.Clinical science (London, England : 1979) · 2022Article
- Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021Review
- Full methylation of H3K27 by PRC2 is dispensable for initial embryoid body formation but required to maintain differentiated cell identity.Development (Cambridge, England) · 2021Article
- Transcriptional regulation by methyltransferases and their role in the heart: highlighting novel emerging functionality.American journal of physiology. Heart and circulatory physiology · 2020Review
- Mechanisms of Neonatal Heart Regeneration.Current cardiology reports · 2020Review
- Age-Related Pathways in Cardiac Regeneration: A Role for lncRNAs?Frontiers in physiology · 2020Review
- H3K27me3-mediated silencing of structural genes is required for zebrafish heart regeneration.Development (Cambridge, England) · 2019Article
- Decellularized neonatal cardiac extracellular matrix prevents widespread ventricular remodeling in adult mammals after myocardial infarction.Acta biomaterialia · 2019Article
- Neonatal Heart Regeneration: Comprehensive Literature Review.Circulation · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neonatal mouse heart has the remarkable capacity to regenerate lost myocardium within the first week of life. Neonatal cardiomyocytes re-express fetal genes that control cell proliferation after injury to promote regeneration. The loss of regenerative capacity of the heart one week after birth coincides with repression of a fetal transcriptional program coordinated by epigenetic regulators. The histone methyltransferase enhancer of zeste homolog 2 (Ezh2) is a repressor of fetal cardiac transcriptional programs and suppresses cardiomyocyte cell proliferation, suggesting a potential function in heart regeneration. However, it was recently demonstrated that Ezh2 is dispensable for heart regeneration in the neonatal heart. Here, we provide evidence supporting this finding and demonstrate that Ezh2 deficiency does not affect regeneration of the neonatal heart. We inactivated Ezh2 in differentiating embryonic cardiomyocytes, which led to depletion of histone H3 trimethylated at lysine 27 (H3K27me3). Ezh2 deficiency in cardiomyocytes did not affect clearance of the fibrotic scar in myocardial infarction (MI) and apical resection models of cardiac injury at post-natal day 1 (P1). Similarly, cardiomyocyte-specific loss of Ezh2 did not affect fibrotic scar size after MI or apical resection at P7, suggesting that it does not extend the regenerative time window. Our results demonstrate that Ezh2 is not required for innate neonatal cardiac regeneration.
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