ArticleGlia2015
Fibroblast growth factor signaling in oligodendrocyte-lineage cells facilitates recovery of chronically demyelinated lesions but is redundant in acute lesions.
Article in Glia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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
39 citing papers in PubMed, 57 citations in OpenAlex.
- Growth Differentiation Factor 11 Is a Circulating Regulator of Oligodendrocyte Differentiation and CNS Myelin Formation and Repair.CNS neuroscience & therapeutics · 2026Article
- Article
- Glial Cells as Key Mediators in the Pathophysiology of Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Spatial transcriptomics reveal heterogeneous cell‒cell interactions among brain regions in cuprizone model consistent with multiple sclerosis lesions.Frontiers in bioinformatics · 2026Article
- Article
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- The FGFR inhibitor Rogaratinib reduces microglia reactivity and synaptic loss in TBI.Frontiers in immunology · 2024Article
- FGF/FGFR system in the central nervous system demyelinating disease: Recent progress and implications for multiple sclerosis.CNS neuroscience & therapeutics · 2023Review
- Biomaterial-Based bFGF Delivery for Nerve Repair.Oxidative medicine and cellular longevity · 2023Review
- Comprehensive visualization of cell-cell interactions in single-cell and spatial transcriptomics with NICHES.Bioinformatics (Oxford, England) · 2023Article
- Interferon Beta-1a versus Combined Interferon Beta-1a and Oligodendrocyte-Specific FGFR1 Deletion in Experimental Autoimmune Encephalomyelitis.International journal of molecular sciences · 2022Article
- A Narrative Review on Axonal Neuroprotection in Multiple Sclerosis.Neurology and therapy · 2022Review
- Retinal ganglion cell expression of cytokine enhances occupancy of NG2 cell-derived astrocytes at the nerve injury site: Implication for axon regeneration.Experimental neurology · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- The relationships between neuroglial and neuronal changes in Alzheimer's disease, and the related controversies II:Journal of central nervous system disease · 2022Review
- Therapeutic Potential of Cytokines in Demyelinating Lesions After Stroke.Journal of molecular neuroscience : MN · 2021Review
- Oligodendrocyte-Specific Deletion ofInternational journal of molecular sciences · 2021Article
- Fibroblast Growth Factor Signalling in the Diseased Nervous System.Molecular neurobiology · 2021Review
- Review
- Treg cell-derived osteopontin promotes microglia-mediated white matter repair after ischemic stroke.Immunity · 2021Article
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
Abstract
Remyelination is a potent regenerative process in demyelinating diseases, such as multiple sclerosis, the effective therapeutic promotion of which will fill an unmet clinical need. The development of proregenerative therapies requires the identification of key regulatory targets that are likely to be involved in the integration of multiple signaling mechanisms. Fibroblast growth factor (FGF) signaling system, which comprises multiple ligands and receptors, potentially provides one such target. Since the FGF/FGF receptor (FGFR) interactions are complex and regulate multiple diverse functions of oligodendrocyte lineage cells, it is difficult to predict their overall therapeutic potential in the regeneration of oligodendrocytes and myelin. Therefore, to assess the integrated effects of FGFR signaling on this process, we simultaneously inactivated both FGFR1 and FGFR2 in oligodendrocytes and their precursors using two Cre-driver mouse lines. Acute and chronic cuprizone-induced or lysolecithin-induced demyelination was established in Fgfr1/Fgfr2 double knockout mice (dKO). We found that in the acute cuprizone model, there was normal differentiation of oligodendrocytes and recovery of myelin in the corpus callosum of both control and dKO mice. Similarly, in the spinal cord, lysolecithin-induced demyelinated lesions regenerated similarly in the dKO and control mice. In contrast, in the chronic cuprizone model, fewer differentiated oligodendrocytes and less efficient myelin recovery were observed in the dKO compared to control mice. These data suggest that while cell-autonomous FGF signaling is redundant during recovery of acute demyelinated lesions, it facilitates regenerative processes in chronic demyelination. Thus, FGF-based therapies have potential value in stimulating oligodendrocyte and myelin regeneration in late-stage disease.
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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.