ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2021
Sustained ErbB Activation Causes Demyelination and Hypomyelination by Driving Necroptosis of Mature Oligodendrocytes and Apoptosis of Oligodendrocyte Precursor Cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- ErbB signaling in brain injury regeneration: Pathway interactions and therapeutic potential.Neural regeneration research · 2026Article
- SOX10 Overexpression Enhances the Oligodendrocyte Lineage Commitment of iOPCs In Vitro by Reshaping Their Chromatin Binding Landscape.Bioengineering (Basel, Switzerland) · 2026Article
- Glial cell deficits are a key feature of schizophrenia: implications for neuronal circuit maintenance and histological differentiation from classical neurodegeneration.Molecular psychiatry · 2025Review
- Comprehensive bioinformatics analysis identifies hub genes associated with immune cell infiltration in early-onset schizophrenia.BMC psychiatry · 2025Article
- Identification of Necroptosis and Immune Infiltration in Heart Failure Through Bioinformatics Analysis.Journal of inflammation research · 2025Article
- Glial interactions in the formation and plasticity of the corpus callosum.Frontiers in cellular neuroscience · 2025Review
- CircRNA-mediated heterogeneous ceRNA regulation mechanism in periodontitis and peri-implantitis.European journal of medical research · 2024Article
- Pan-ErbB inhibition impairs cognition via disrupting myelination and aerobic glycolysis in oligodendrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Antidepressant effect of teriflunomide via oligodendrocyte protection in a mouse model.Heliyon · 2024Article
- The Genomic Intersection of Oligodendrocyte Dynamics in Schizophrenia and Aging Unravels Novel Pathological Mechanisms and Therapeutic Potentials.International journal of molecular sciences · 2024Review
- Microglia regulation of central nervous system myelin health and regeneration.Nature reviews. Immunology · 2024Review
- Investigating EGF and PAG1 as necroptosis-related biomarkers for diabetic nephropathy: anAging · 2023Article
- Evidence That DDR1 Promotes Oligodendrocyte Differentiation during Development and Myelin Repair after Injury.International journal of molecular sciences · 2023Article
- Role of hypoxic exosomes and the mechanisms of exosome release in the CNS under hypoxic conditions.Frontiers in neurology · 2023Review
- Epidermal Growth Factor Pathway in the Age-Related Decline of Oligodendrocyte Regeneration.Frontiers in cellular neuroscience · 2022Review
- Early Brain microRNA/mRNA Expression is Region-Specific After Neonatal Hypoxic-Ischemic Injury in a Mouse Model.Frontiers in genetics · 2022Article
- Extreme Glycemic Fluctuations Debilitate NRG1, ErbB Receptors and Olig1 Function: Association with Regeneration, Cognition and Mood Alterations During Diabetes.Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oligodendrocytes are vulnerable to genetic and environmental insults and its injury leads to demyelinating diseases. The roles of ErbB receptors in maintaining the CNS myelin integrity are largely unknown. Here, we overactivate ErbB receptors that mediate signaling of either neuregulin (NRG) or epidermal growth factor (EGF) family growth factors and found their synergistic activation caused deleterious outcomes in white matter. Sustained ErbB activation induced by the tetracycline-dependent mouse tool
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Registered trials
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.