ArticleExperimental neurology2014
Inhibitors of myelination: ECM changes, CSPGs and PTPs.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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
48 citing papers in PubMed, 73 citations in OpenAlex.
- Extrinsic Regulation of Optic Nerve Axon Regeneration in the Adult Central Nervous System.Cells · 2026Review
- Review
- [Research advances in the inhibitory effect of chondroitin sulfate proteoglycans on axon growth after premature white matter injury and its underlying mechanisms].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- Exosomes: a promising microenvironment modulator for spinal cord injury treatment.International journal of biological sciences · 2025Review
- Developmental exposure of zebrafish to saxitoxin causes altered expression of genes associated with axonal growth.Neurotoxicology · 2024Article
- Schwann Cell-Derived Exosomes Induced Axon Growth after Spinal Cord Injury by Decreasing PTP-σ Activation on CSPGs via the Rho/ROCK Pathway.Neurochemical research · 2024Article
- Loss of miR-145 promotes remyelination and functional recovery in a model of chronic central demyelination.Communications biology · 2024Article
- Inflammation in multiple sclerosis: consequences for remyelination and disease progression.Nature reviews. Neurology · 2023Review
- Cannabinoid CBCell death & disease · 2022Article
- Progression in translational research on spinal cord injury based on microenvironment imbalance.Bone research · 2022Review
- Oligodendrocyte and Extracellular Matrix Contributions to Central Nervous System Motor Function: Implications for Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2022Review
- Remyelination in PNS and CNS: current and upcoming cellular and molecular strategies to treat disabling neuropathies.Molecular biology reports · 2021Review
- Transcriptional Alterations in Dorsolateral Prefrontal Cortex and Nucleus Accumbens Implicate Neuroinflammation and Synaptic Remodeling in Opioid Use Disorder.Biological psychiatry · 2021Article
- The extracellular matrix as modifier of neuroinflammation and remyelination in multiple sclerosis.Brain : a journal of neurology · 2021Review
- THAP1 modulates oligodendrocyte maturation by regulating ECM degradation in lysosomes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The CNS/PNS Extracellular Matrix Provides Instructive Guidance Cues to Neural Cells and Neuroregulatory Proteins in Neural Development and Repair.International journal of molecular sciences · 2021Review
- GDE2 expression in oligodendroglia regulates the pace of oligodendrocyte maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Select neurotrophins promote oligodendrocyte progenitor cell process outgrowth in the presence of chondroitin sulfate proteoglycans.Journal of neuroscience research · 2021Article
- Overcoming the inhibitory microenvironment surrounding oligodendrocyte progenitor cells following experimental demyelination.Nature communications · 2021Article
- Impairing committed cholesterol biosynthesis in white matter astrocytes, but not grey matter astrocytes, enhances in vitro myelination.Journal of neurochemistry · 2021Article
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2 authors at 1 institution in 1 country.
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Abstract
After inflammation-induced demyelination, such as in the disease multiple sclerosis, endogenous remyelination often fails. However, in animal models of demyelination induced with toxins, remyelination can be quite robust. A significant difference between inflammation-induced and toxin-induced demyelination is the response of local cells within the lesion, including astrocytes, oligodendrocytes, microglia/macrophages, and NG2+ cells, which respond to inflammatory stimuli with increased extracellular matrix (ECM) protein and chondroitin sulfate proteoglycan (CSPG) production and deposition. Here, we summarize current knowledge of ECM changes in demyelinating lesions, as well as oligodendrocyte responses to aberrant ECM proteins and CSPGs after various types of demyelinating insults. The discovery that CSPGs act through the receptor protein tyrosine phosphatase sigma (PTPσ) and the Rho-ROCK pathway to inhibit oligodendrocyte process extension and myelination, but not oligodendrocyte differentiation (Pendleton et al., Experimental Neurology (2013) vol. 247, pp. 113-121), highlights the need to better understand the ECM changes that accompany demyelination and their influence on oligodendrocytes and effective remyelination.
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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 Socratic graph.