ReviewFrontiers in molecular neuroscience2017
MeCP2 Deficiency in Neuroglia: New Progress in the Pathogenesis of Rett Syndrome.
Review in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 55 citations in OpenAlex.
- Epigenetic changes associated with the progression of prion disease in Syrian hamsters (Prion · 2026Article
- Rett syndrome: MECP2 biology, multisystem pathophysiology, and the evolving therapeutic landscape.European journal of pediatrics · 2026Review
- Single-nucleus profiling reveals a core disease signature and cell type-specific vulnerabilities in early Rett syndrome.Science advances · 2026Article
- Defective ventral neurogenesis due to midfetal Chd8 mutation drives autistic-like behavior in mice.Nature communications · 2026Article
- Early differential impact of MeCP2 mutations on functional networks in Rett syndrome patient-derived human cortical organoids.Nature communications · 2026Article
- Ethanol Alters DNMT1/3a/3b Expression Profile, Promotes Persistent DNA Hypomethylation in Human Brain Endothelial Cells and Impairs Late Cortical Angiogenesis.Journal of neurochemistry · 2026Article
- Article
- Epigenetic Changes Associated with the Progression of Prion Disease in Syrian Hamsters (Mesocricetus auratus).Research square · 2025Article
- Microglial deficiency in the ATRX chromatin remodeler elicits a viral mimicry immune response that impacts neuronal function and behavior.PLoS biology · 2025Article
- MeCP2 Lactylation Protects against Ischemic Brain Injury by Transcriptionally Regulating Neuronal Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- An Astrocyte Transplantation Method to Investigate Astrocyte Development and Diversity in the Central Nervous System (CNS).Methods in molecular biology (Clifton, N.J.) · 2025Article
- Mitochondrial dysfunction and increased reactive oxygen species production in MECP2 mutant astrocytes and their impact on neurons.Scientific reports · 2024Article
- Modulation of Brain Cholesterol Metabolism through CYP46A1 Overexpression for Rett Syndrome.Pharmaceutics · 2024Article
- Downregulated SPESP1-driven fibroblast senescence decreases wound healing in aged mice.Clinical and translational medicine · 2024Article
- Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023Review
- MeCP2 dysfunction prevents proper BMP signaling and neural progenitor expansion in brain organoid.Annals of clinical and translational neurology · 2023Article
- Astrocytes Transplanted during Early Postnatal Development Integrate, Mature, and Survive Long Term in Mouse Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Serum Neurofilament Light Chain and Glial Fibrillary Acidic Protein as Potential Diagnostic Biomarkers in Autism Spectrum Disorders: A Preliminary Study.International journal of molecular sciences · 2023Article
- Global Impairment of Immediate-Early Genes Expression in Rett Syndrome Models and Patients Linked to Myelination Defects.International journal of molecular sciences · 2023Article
- Advances in the pathogenesis of Rett syndrome using cell models.Animal models and experimental medicine · 2022Review
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
Rett syndrome (RTT) is an X-linked neurodevelopmental disease predominantly caused by mutations of the methyl-CpG-binding protein 2 (MeCP2) gene. Generally, RTT has been attributed to neuron-centric dysfunction. However, increasing evidence has shown that glial abnormalities are also involved in the pathogenesis of RTT. Mice that are MeCP2-null specifically in glial cells showed similar behavioral and/or neuronal abnormalities as those found in MeCP2-null mice, a mouse model of RTT. MeCP2 deficiency in astrocytes impacts the expression of glial intermediate filament proteins such as fibrillary acidic protein (GFAP) and S100 and induces neuron toxicity by disturbing glutamate metabolism or enhancing microtubule instability. MeCP2 deficiency in oligodendrocytes (OLs) results in down-regulation of myelin gene expression and impacts myelination. While MeCP2-deficient microglia cells fail in response to environmental stimuli, release excessive glutamate, and aggravate impairment of the neuronal circuit. In this review, we mainly focus on the progress in determining the role of MeCP2 in glial cells involved in RTT, which may provide further insight into a therapeutic intervention for RTT.
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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.