ReviewGlia2022
The roles of microglia and astrocytes in phagocytosis and myelination: Insights from the cuprizone model of multiple sclerosis.
Review in Glia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- Systematic review of photobiomodulation for multiple sclerosis.Frontiers in neurology · 2024Pooled it
- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- Neuroprotective effects of glucotropaeolin as the major glucosinolate of cress seed on cuprizone-induced mouse model of multiple sclerosis.Biochemistry and biophysics reports · 2026Article
- Neurological impairment in long COVID: implications for neurodegenerative disease.Journal of translational medicine · 2026Review
- Brain targeting and trafficking of extracellular vesicles in central nervous system diseases: a therapeutic roadmap.Nanomedicine (London, England) · 2026Review
- Astrocyte-specific NRCAM deficiency promotes GABAergic synapse pruning to drive central sensitization in bone cancer pain.Journal of translational medicine · 2026Article
- T cell-targeted immunotherapies for multiple sclerosis: molecular mechanisms to therapeutic perspectives from Traditional Chinese medicine.Acta pharmacologica Sinica · 2026Article
- Cannabinoid CBCell communication and signaling : CCS · 2026Article
- Adjunctive strategies in multiple sclerosis treatment: non-pharmacological approaches and their potential clinical implications.Journal of translational medicine · 2026Review
- Effects of Maternal Tetramethyl Bisphenol F Exposure on Neurodevelopment and Behavior in Mouse Offspring.International journal of molecular sciences · 2026Article
- A Novel Central-Peripheral Interface: The Auditory Nerve Glial Transition Zone Exhibits Enhanced Age-Related Immune and Glial Cell Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- TGF-β-induced fibrotic scar formation limits recovery of spinal cord injury.Bone research · 2026Article
- Article
- The effect of astrocyte depletion and repopulation approaches in pathological condition of CNS.Acta neurologica Belgica · 2026Review
- Exosomes as mediators of repair and immunoregulation in multiple sclerosis: a new frontier in cell-free therapy.Molecular biology reports · 2026Review
- Bone marrow mesenchymal stem cells ameliorate intermittent multiple sclerosis: quantitative cerebellar microscopy and functional analysis in cuprizone-induced mice.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Glial Cells as Key Mediators in the Pathophysiology of Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Microglia Mitochondrial Metabolism in Neurological Diseases.Molecular neurobiology · 2026Review
- Article
- Baicalein alleviates long-term cognitive impairments induced by repeated neonatal sevoflurane exposure via inhibition of cortical microglial TLR4/NF-kB signaling.Brain, behavior, & immunity - health · 2025Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In human demyelinating diseases such as multiple sclerosis (MS), an imbalance between demyelination and remyelination can trigger progressive degenerative processes. The clearance of myelin debris (phagocytosis) from the site of demyelination by microglia is critically important to achieve adequate remyelination and to slow the progression of the disease. However, how microglia phagocytose the myelin debris, and why clearance is impaired in MS, is not fully known; likewise, the role of the microglia in remyelination remains unclear. Recent studies using cuprizone (CPZ) as an animal model of central nervous system demyelination revealed that the up-regulation of signaling proteins in microglia facilitates effective phagocytosis of myelin debris. Moreover, during demyelination, protective mediators are released from activated microglia, resulting in the acceleration of remyelination in the CPZ model. In contrast, inadequate microglial activation or recruitment to the site of demyelination, and the production of toxic mediators, impairs remyelination resulting in progressive demyelination. In addition to the microglia-mediated phagocytosis, astrocytes play an important role in the phagocytic process by recruiting microglia to the site of demyelination and producing regenerative mediators. The current review is an update of these emerging findings from the CPZ animal model, discussing the roles of microglia and astrocytes in phagocytosis and myelination.
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What OpenQuestion holds
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.