ArticleThe Journal of experimental medicine2020
Pro-inflammatory activation following demyelination is required for myelin clearance and oligodendrogenesis.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.
- Immunoregulation of Glia after spinal cord injury: a bibliometric analysis.Frontiers in immunology · 2024Pooled it
- Review
- M2-associated microglial states in oligodendrocyte regulation and white matter repair in vascular dementia.Journal of translational medicine · 2026Review
- Reduced LACTB expression in myeloid cells is associated with elevated succinylcarnitine and reduced Alzheimer's disease risk.Research square · 2026Article
- Melatonin promotes recovery from ischemic stroke by modulating microglia polarization and inhibiting oligodendrocyte pyroptosis via the RORα/AMPKα/STAT1 pathway.Journal of translational medicine · 2026Article
- Myelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside.Medicina (Kaunas, Lithuania) · 2026Review
- 18:2 Cholesterol Ester is a Novel Prognostic Biomarker of Disease Progression in Multiple Sclerosis.Molecular neurobiology · 2026Article
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 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
- Chaperone-mediated autophagy sustains pericyte stemness necessary for brain tissue homeostasis.Journal of advanced research · 2026Article
- TREM2 expression level is critical for microglial state, metabolic capacity and efficacy of TREM2 agonism.Nature communications · 2026Article
- Mitochondrial microprotein MOCCI controls neuroinflammation by altering glial activation states.Frontiers in immunology · 2026Article
- Integrating bioinformatic prediction and the "gut microbiota-inflammation-skin axis" to decipher the mechanisms of quercetin (fromFrontiers in immunology · 2026Article
- From scavenger to victim: mechanism and treatment of microglial ferroptosis in white matter injury disease.Frontiers in immunology · 2026Review
- Article
- The auditory nerve glial transition zone is a focal site of age-related immune-myelin interactions.Frontiers in immunology · 2026Article
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Quaking Protein in Myelin Maintenance and Regeneration in the Central Nervous System.Molecular neurobiology · 2025Review
- Label-free nonlinear microscopy probes cellular metabolism and myelin dynamics in live tissue.Communications biology · 2025Article
- Age-impaired remyelination is associated with dysregulated microglial transitions.Nature communications · 2025Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remyelination requires innate immune system function, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammatory NF-κB-dependent activation in phagocytes occurs rapidly after myelin injury. We found that the pro-inflammatory response depends on myeloid differentiation primary response 88 (MyD88). MyD88-deficient mice and zebrafish were not only impaired in the degradation of myelin debris, but also in initiating the generation of new oligodendrocytes for myelin repair. We identified reduced generation of TNF-α in lesions of MyD88-deficient animals, a pro-inflammatory molecule that was able to induce the generation of new premyelinating oligodendrocytes. Our study shows that pro-inflammatory phagocytic signaling is required for myelin debris degradation, for inflammation resolution, and for initiating the generation of new oligodendrocytes.
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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.