ArticlePharmaceuticals (Basel, Switzerland)2021
Dysregulation of Blood-Brain Barrier and Exacerbated Inflammatory Response in Cx47-Deficient Mice after Induction of EAE.
Article in Pharmaceuticals (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- The Breakdown of Neurovascular Barriers: Molecular Mechanisms of Tight Junction Dysfunction.Molecular neurobiology · 2025Review
- Early olfactory dysfunction in experimental autoimmune encephalomyelitis reflects transient brain barrier breach and initiation of neuroinflammation in the olfactory bulb.Frontiers in cellular neuroscience · 2025Article
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Astroglial connexin 43 is a novel therapeutic target for chronic multiple sclerosis model.Scientific reports · 2024Article
- Sigma-1 Receptor Inhibition Reduces Mechanical Allodynia and Modulate Neuroinflammation in Chronic Neuropathic Pain.Molecular neurobiology · 2024Article
- Fasudil-modified macrophages reduce inflammation and regulate the immune response in experimental autoimmune encephalomyelitis.Neural regeneration research · 2024Article
- Connexins Control Glial Inflammation in Various Neurological Diseases.International journal of molecular sciences · 2023Review
- Mechanisms of Diseases Associated with Mutation in GJC2/Connexin 47.Biomolecules · 2023Review
- Interactions Between Astrocytes and Oligodendroglia in Myelin Development and Related Brain Diseases.Neuroscience bulletin · 2023Review
- Upregulation of C-X-C motif chemokine 12 in the spinal cord alleviated the symptoms of experimental autoimmune encephalomyelitis in Lewis rats.Frontiers in neuroscience · 2023Article
- GJA1/CX43 High Expression Levels in the Cervical Spinal Cord of ALS Patients Correlate to Microglia-Mediated Neuroinflammatory Profile.Biomedicines · 2022Article
- Beneficial Effect of Melatonin Alone or in Combination with Glatiramer Acetate and Interferon β-1b on Experimental Autoimmune Encephalomyelitis.Molecules (Basel, Switzerland) · 2022Article
- Cytokines in the Brain and Neuroinflammation: We Didn't Starve the Fire!Pharmaceuticals (Basel, Switzerland) · 2022Review
- Design of Oral Sustained-Release Pellets by Modeling and Simulation Approach to Improve Compliance for Repurposing Sobrerol.Pharmaceutics · 2022Article
- Advantages and limitations of experimental autoimmune encephalomyelitis in breaking down the role of the gut microbiome in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Induction of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), in connexin 32 (Cx32) or Cx47 knockout (KO) mice with deficiency in oligodendrocyte gap junctions (GJs) results in a more severe disease course. In particular, Cx47 KO EAE mice experience an earlier EAE onset and more pronounced disease severity, accompanied by dysregulated pro-inflammatory responses preceding the disease manifestations. In this study, analysis of relevant pro-inflammatory cytokines in wild type EAE, Cx32 KO EAE, and Cx47 KO EAE mice revealed altered expression of
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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.