ArticleJournal of neuroinflammation2024
Inflammation-induced TRPV4 channels exacerbate blood-brain barrier dysfunction in multiple sclerosis.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Elusive B Cell Antigen in Multiple Sclerosis: Time to Rethink CNS B Cell Functions.International journal of molecular sciences · 2025Pooled it
- Friend or foe? Glial-vascular interactions in health and neurodegenerative disease.Pharmacological reviews · 2026Review
- 25+ Years of TRPV4: From Discovery to Translational Horizons.Research square · 2026Article
- T cell-targeted immunotherapies for multiple sclerosis: molecular mechanisms to therapeutic perspectives from Traditional Chinese medicine.Acta pharmacologica Sinica · 2026Article
- Multiplexed Tandem Mass Spectrometry Imaging Enables Large-Scale Isomer Mapping and Annotation in Tissues.Angewandte Chemie (International ed. in English) · 2026Article
- Microglial Innate Immune Memory: Implications and Research Advances in Central Nervous System Disorders.Current issues in molecular biology · 2026Review
- The role of TRPV4 in ischemic stroke.Molecular brain · 2026Review
- Cerebrospinal fluid mechanics across CNS barriers: from production, circulation, and clearance to mechanomedicine.Frontiers in neuroscience · 2026Review
- Smoldering neuroinflammation in progressive multiple sclerosis: mechanisms, imaging biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- The immune-endothelial axis in neurovascular pathophysiology: a framework for targeted interventions.Frontiers in immunology · 2026Review
- Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- Flecainide mediated sodium channel blockade enhances blood brain barrier integrity and promotes neuroprotection in neuroinflammation.Scientific reports · 2025Article
- Relationship between blood-cerebrospinal fluid barrier integrity, cardiometabolic, and inflammatory factors in schizophrenia-spectrum disorders.Brain, behavior, & immunity - health · 2025Article
- Inflammation alters myeloid cell and oligodendroglial iron-handling in multiple sclerosis.Acta neuropathologica communications · 2025Article
- Spatial mapping of the AA-PGEActa neuropathologica · 2025Article
- Transient receptor potential vanilloid 4 blockage attenuates pyroptosis in hippocampus of mice following pilocarpine‑induced status epilepticus.Acta neuropathologica communications · 2025Article
- Review
- Endothelial-Ercc1 DNA repair deficiency provokes blood-brain barrier dysfunction.Cell death & disease · 2025Article
- A QUARTER CENTURY OF CALCIUM-PERMEABLE ION CHANNEL, TRPV4: PERSPECTIVES ON EXPRESSION AND FUNCTION IN ENDOTHELIAL CELLS-TIME TO TRANSLATE.Transactions of the American Clinical and Climatological Association · 2025Review
- Brain-derived extracellular vesicles potentially mediate crosstalk with peripheral organs in neurodegenerative diseases.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 6 countries.
Funding
Abstract
backgroundBlood-brain barrier (BBB) dysfunction and immune cell migration into the central nervous system (CNS) are pathogenic drivers of multiple sclerosis (MS). Ways to reinstate BBB function and subsequently limit neuroinflammation present promising strategies to restrict disease progression. However, to date, the molecular players directing BBB impairment in MS remain poorly understood. One suggested candidate to impact BBB function is the transient receptor potential vanilloid-type 4 ion channel (TRPV4), but its specific role in MS pathogenesis remains unclear. Here, we investigated the role of TRPV4 in BBB dysfunction in MS. MAIN TEXT: In human post-mortem MS brain tissue, we observed a region-specific increase in endothelial TRPV4 expression around mixed active/inactive lesions, which coincided with perivascular microglia enrichment in the same area. Using in vitro models, we identified that microglia-derived tumor necrosis factor-α (TNFα) induced brain endothelial TRPV4 expression. Also, we found that TRPV4 levels influenced brain endothelial barrier formation via expression of the brain endothelial tight junction molecule claudin-5. In contrast, during an inflammatory insult, TRPV4 promoted a pathological endothelial molecular signature, as evidenced by enhanced expression of inflammatory mediators and cell adhesion molecules. Moreover, TRPV4 activity mediated T cell extravasation across the brain endothelium.
conclusionCollectively, our findings suggest a novel role for endothelial TRPV4 in MS, in which enhanced expression contributes to MS pathogenesis by driving BBB dysfunction and immune cell migration.
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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.