ArticleNature communications2016
An inhibitor of chondroitin sulfate proteoglycan synthesis promotes central nervous system remyelination.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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
120 citing papers in PubMed, 202 citations in OpenAlex.
- The role of type I collagen in white matter injury.Anatomical science international · 2026Review
- Heparan sulfate and glycomimetics: Advances in synthesis and biological applications for post-stroke neurorepair.Neuroprotection (Chichester, England) · 2026Review
- Eriochrome Cyanine R revisited: a standardized myelin stain protocol for thick sections of the central & peripheral nervous system across species, pathologies and disease models.Brain structure & function · 2026Article
- Neuregulin-1 facilitates myelin regeneration through microglia-mediated mechanisms in a mouse model of chronic demyelination.Nature communications · 2026Article
- Routes of precursors' migration in remyelination.Brain : a journal of neurology · 2026Review
- Synthesis and Antiproliferative Activity of FluorinatedThe Journal of organic chemistry · 2026Article
- Chondroitin Sulfate Proteoglycans in CNS Development and Pathophysiology.Journal of neuroscience research · 2026Review
- Post-ischemic modification of neurogenesis and oligodendrogenesis in rodent models.Frontiers in neural circuits · 2026Review
- The oxidative stress-inflammation self-perpetuating cycle in multiple sclerosis: from mechanisms to emerging antioxidant strategies.Frontiers in pharmacology · 2026Review
- Disrupting CSPG-Driven Microglia-Astrocyte Crosstalk Enables Scar-Free Repair in Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Evaluating the CRP Interactome: Insights into Possible Novel Roles in Cellular Signaling and Tumorigenicity.Current issues in molecular biology · 2025Review
- The molecular mechanism of uptake and cell-to-cell transmission of arginine-containing dipeptide repeat proteins.bioRxiv : the preprint server for biology · 2025Article
- A focus on the normal-appearing white and gray matter within the multiple sclerosis brain: a link to smoldering progression.Acta neuropathologica · 2025Review
- The Future of PET Imaging in Multiple Sclerosis: Characterisation of Individual White Matter Lesions.Journal of clinical medicine · 2025Review
- Blood-Brain Barrier (BBB) Dysfunction in CNS Diseases: Paying Attention to Pericytes.CNS neuroscience & therapeutics · 2025Review
- Review
- Article
- Article
- Loss of miR-145 promotes remyelination and functional recovery in a model of chronic central demyelination.Communications biology · 2024Article
60 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
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remyelination is the generation of new myelin sheaths after injury facilitated by processes of differentiating oligodendrocyte precursor cells (OPCs). Although this repair phenomenon occurs in lesions of multiple sclerosis patients, many lesions fail to completely remyelinate. A number of factors have been identified that contribute to remyelination failure, including the upregulated chondroitin sulfate proteoglycans (CSPGs) that comprise part of the astrogliotic scar. We show that in vitro, OPCs have dramatically reduced process outgrowth in the presence of CSPGs, and a medication library that includes a number of recently reported OPC differentiation drugs failed to rescue this inhibitory phenotype on CSPGs. We introduce a novel CSPG synthesis inhibitor to reduce CSPG content and find rescued process outgrowth from OPCs in vitro and accelerated remyelination following focal demyelination in mice. Preventing CSPG deposition into the lesion microenvironment may be a useful strategy to promote repair in multiple sclerosis and other neurological disorders.
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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.