ReviewChannels (Austin, Tex.)2019
The role of oligodendrocyte gap junctions in neuroinflammation.
Review in Channels (Austin, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Two Cases of Multiple Sclerosis in a Family With X-Linked Charcot-Marie-Tooth Disease.Neurology. Genetics · 2026Article
- Spatial Transcriptomics Reveals a T Cell-Mediated Microglial Activation Axis of Immune Checkpoint Inhibition-Related Adverse Events in the Brain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Maackiain Reduces Neuroinflammation by Modulating Inflammatory Signals in LPS-InducedJournal of microbiology and biotechnology · 2026Article
- Astroglial connexin 43 is a novel therapeutic target for chronic multiple sclerosis model.Scientific reports · 2024Article
- Fatal leukodystrophy in Costello syndrome: a case report.BMC pediatrics · 2023Article
- The Structure and Function of Glial Networks: Beyond the Neuronal Connections.Neuroscience bulletin · 2023Review
- Potentially toxic elements in the brains of people with multiple sclerosis.Scientific reports · 2023Article
- Enhancing axonal myelination in seniors: A review exploring the potential impact cannabis has on myelination in the aged brain.Frontiers in aging neuroscience · 2023Review
- Glial Gap Junction Pathology in the Spinal Cord of the 5xFAD Mouse Model of Early-Onset Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Lumbar spine intrathecal transplantation of neural precursor cells promotes oligodendrocyte proliferation in hot spots of chronic demyelination.Brain pathology (Zurich, Switzerland) · 2022Article
- Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways.Antioxidants (Basel, Switzerland) · 2022Review
- Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders.Journal of neuroscience research · 2021Review
- Synaptic Reshaping and Neuronal Outcomes in the Temporal Lobe Epilepsy.International journal of molecular sciences · 2021Review
- Effect of zymosan on the expression and function of the gap-junction protein connexin 43 in human corneal fibroblasts.International journal of ophthalmology · 2021Article
- Multiple sclerosis iPS-derived oligodendroglia conserve their properties to functionally interact with axons and glia in vivo.Science advances · 2020Article
- Review
- Article
- Altered Expression of Glial Gap Junction Proteins Cx43, Cx30, and Cx47 in the 5XFAD Model of Alzheimer's Disease.Frontiers in neuroscience · 2020Article
- The Multifaceted Role of Astrocyte Connexin 43 in Ischemic Stroke Through Forming Hemichannels and Gap Junctions.Frontiers in neurology · 2020Review
- Connexins-Based Hemichannels/Channels and Their Relationship with Inflammation, Seizures and Epilepsy.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gap junctions (GJs) provide channels for direct cell-to-cell connectivity serving the homeostasis in several organs of vertebrates including the central (CNS) and peripheral (PNS) nervous systems. GJs are composed of connexins (Cx), which show a highly distinct cellular and subcellular expression pattern. Oligodendrocytes, the myelinating cells of the CNS, are characterized by extensive GJ connectivity with each other as well as with astrocytes. The main oligodendrocyte connexins forming these GJ channels are Cx47 and Cx32. The importance of these channels has been highlighted by the discovery of human diseases caused by mutations in oligodendrocyte connexins, manifesting with leukodystrophy or transient encephalopathy. Experimental models have provided further evidence that oligodendrocyte GJs are essential for CNS myelination and homeostasis, while a strong inflammatory component has been recognized in the absence of oligodendrocyte connexins. Further studies revealed that connexins are also disrupted in multiple sclerosis (MS) brain, and in experimental models of induced inflammatory demyelination. Moreover, induced demyelination was more severe and associated with higher degree of CNS inflammation in models with oligodendrocyte GJ deficiency, suggesting that disrupted connexin expression in oligodendrocytes is not only a consequence but can also drive a pro-inflammatory environment in acquired demyelinating disorders such as MS. In this review, we summarize the current insights from human disorders as well as from genetic and acquired models of demyelination related to oligodendrocyte connexins, with the remaining challenges and perspectives.
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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.