ArticleCell proliferation2025
Ezh2 Regulates Early Astrocyte Morphogenesis and Influences the Coverage of Astrocytic Endfeet on the Vasculature.
Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- Endothelial-specific Ezh2 deficiency exacerbates blood-brain barrier dysfunction and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- The Role of Astrocyte-Neuron Interactions in Shaping Neuronal Maturation during Human Brain Development.Computational and structural biotechnology journal · 2026Article
- Article
- Comparison of the Effect of the Combination of Sodium Valproate and Sodium Dichloroacetate on the Expression ofPharmaceutics · 2025Article
- Ezh2 Regulates Early Astrocyte Morphogenesis and Influences the Coverage of Astrocytic Endfeet on the Vasculature.Cell proliferation · 2025Article
- Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Astrocytes are crucial for central nervous system (CNS) development and function, with their differentiation being stringently controlled by epigenetic mechanisms, such as histone modifications. Enhancer of Zeste Homologue 2 (EZH2), a histone methyltransferase, is essential for the suppression of gene expression. However, the role of EZH2 in astrocyte early morphogenesis has remained unclear. Using an astrocyte-specific Ezh2 knockout (cKO) mouse model, we examined the effects of EZH2 deletion on astrocyte morphogenesis, blood-brain barrier (BBB) integrity and neurodevelopment. Loss of EZH2 led to increased glial fibrillary acidic protein (GFAP) expression, altered astrocyte morphology and reduced coverage of astrocytic endfeet on blood vessels, compromising BBB integrity. Vascular abnormalities, characterised by increased vascular density and smaller vessel diameter, mirrored compensatory changes seen in moyamoya disease. RNA-sequencing and ChIP-seq identified Ddn as a key upregulated gene in Ezh2
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Registered trials
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