ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Elevated TRPV4 Levels Contribute to Endothelial Damage and Scarring in Experimental Spinal Cord Injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 59 citations in OpenAlex.
- Blood-spinal cord barrier disruption after spinal cord injury: a time-dependent mechanistic review.Frontiers in cellular neuroscience · 2026Review
- From Mechanoelectric Conversion to Tissue Regeneration: Translational Progress in Piezoelectric Materials.Advanced materials (Deerfield Beach, Fla.) · 2025Review
- Loss of TRPV4 is insufficient to promote repair in a spinal cord injury contusion model.Scientific reports · 2025Article
- Activation of Piezo1 and TRPV4 channels contributes to hCMEC/D3 cell mechano-sensing.Frontiers in physiology · 2025Article
- TRPV4-A Multifunctional Cellular Sensor Protein with Therapeutic Potential.Sensors (Basel, Switzerland) · 2024Review
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- Gain-of-function mutations of TRPV4 acting in endothelial cells drive blood-CNS barrier breakdown and motor neuron degeneration in mice.Science translational medicine · 2024Article
- Inflammation-induced TRPV4 channels exacerbate blood-brain barrier dysfunction in multiple sclerosis.Journal of neuroinflammation · 2024Article
- Chondroitin Sulfate Proteoglycans Revisited: Its Mechanism of Generation and Action for Spinal Cord Injury.Aging and disease · 2024Review
- Positive effect of microvascular proliferation on functional recovery in experimental cervical spondylotic myelopathy.Frontiers in neuroscience · 2024Article
- Microvascular endothelial cells derived from spinal cord promote spinal cord injury repair.Bioactive materials · 2023Article
- Review
- The Provenance, Providence, and Position of Endothelial Cells in Injured Spinal Cord Vascular Pathology.Cellular and molecular neurobiology · 2023Review
- Astrocytic TRPV4 Channels and Their Role in Brain Ischemia.International journal of molecular sciences · 2023Review
- TRPV4 Role in Neuropathic Pain Mechanisms in Rodents.Antioxidants (Basel, Switzerland) · 2022Review
- Molecular Mechanisms in the Vascular and Nervous Systems following Traumatic Spinal Cord Injury.Life (Basel, Switzerland) · 2022Review
- Article
- TRPV4: A trigger of pathological RhoA activation in neurological disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Commentary on "The Role of Alginate Hydrogels as a Potential Treatment Modality for Spinal Cord Injury: A Comprehensive Review of the Literature".Neurospine · 2022Article
- Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Currently, the role of transient receptor potential vanilloid type 4 (TRPV4), a nonselective cation channel in the pathology of spinal cord injury (SCI), is not recognized. Herein, we report the expression and contribution of TRPV4 in the pathology of scarring and endothelial and secondary damage after SCI. TRPV4 expression increased during the inflammatory phase in female rats after SCI and was expressed primarily by cells at endothelial-microglial junctions. Two-photon microscopy of intracellular-free Ca
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What OpenQuestion holds
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.