ArticlePloS one2012
Conditional ablation of Ezh2 in murine hearts reveals its essential roles in endocardial cushion formation, cardiomyocyte proliferation and survival.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- Enhancer of zeste homolog 2 (Ezh2) is required in mouse Isl1-expressing progenitors for proper development of cardiac and skeletal hindlimb structures.Biology open · 2026Article
- Article
- EZH2 variants derived from cryptic splice sites govern distinct epigenetic patterns during embryonic development.Nucleic acids research · 2025Article
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- Role of EZH2-mediated epigenetic modification on vascular smooth muscle in cardiovascular diseases: A mini-review.Frontiers in pharmacology · 2024Review
- The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023Review
- EZH2 controls epicardial cell migration during heart development.Life science alliance · 2023Article
- EZH2 modulates retinoic acid signaling to ensure myotube formation during development.FEBS letters · 2022Article
- Epigenetics in Congenital Heart Disease.Journal of the American Heart Association · 2022Review
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Genetic and epigenetic mechanisms in the development of congenital heart diseases.World journal of pediatric surgery · 2021Review
- 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
- Identification and Expression Pattern of EZH2 in Pig Developing Fetuses.BioMed research international · 2020Article
- Epigenetics and Mechanobiology in Heart Development and Congenital Heart Disease.Diseases (Basel, Switzerland) · 2019Review
- The histone methyltransferase EZH2 is required for normal uterine development and function in mice†.Biology of reproduction · 2019Article
- Exosomes from Suxiao Jiuxin pill-treated cardiac mesenchymal stem cells decrease H3K27 demethylase UTX expression in mouse cardiomyocytes in vitro.Acta pharmacologica Sinica · 2018Article
- Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration.Nature communications · 2018Article
- Article
- Divergent Requirements for EZH1 in Heart Development Versus Regeneration.Circulation research · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ezh2 is a histone trimethyltransferase that silences genes mainly via catalyzing trimethylation of histone 3 lysine 27 (H3K27Me3). The role of Ezh2 as a regulator of gene silencing and cell proliferation in cancer development has been extensively investigated; however, its function in heart development during embryonic cardiogenesis has not been well studied. In the present study, we used a genetically modified mouse system in which Ezh2 was specifically ablated in the mouse heart. We identified a wide spectrum of cardiovascular malformations in the Ezh2 mutant mice, which collectively led to perinatal death. In the Ezh2 mutant heart, the endocardial cushions (ECs) were hypoplastic and the endothelial-to-mesenchymal transition (EMT) process was impaired. The hearts of Ezh2 mutant mice also exhibited decreased cardiomyocyte proliferation and increased apoptosis. We further identified that the Hey2 gene, which is important for cardiomyocyte proliferation and cardiac morphogenesis, is a downstream target of Ezh2. The regulation of Hey2 expression by Ezh2 may be independent of Notch signaling activity. Our work defines an indispensible role of the chromatin remodeling factor Ezh2 in normal cardiovascular development.
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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.