ArticleFrontiers in cellular neuroscience2022
Lack of NHE6 and Inhibition of NKCC1 Associated With Increased Permeability in Blood Labyrinth Barrier-Derived Endothelial Cell Layer.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- The Gut-Ear Axis: From Dysbiosis to Auditory and Vestibular Disorders.International journal of molecular sciences · 2026Review
- The Recycling Endosomal (NaActa physiologica (Oxford, England) · 2026Article
- How Effective are Exosomes in Overcoming Blood-Labyrinth Barrier in Sensorineural Hearing Loss? A Comprehensive Review of the Literature.International journal of nanomedicine · 2026Review
- Engineering exosomes in the treatment of sensorineural hearing loss: from basic research to clinical applications.Frontiers in molecular neuroscience · 2026Review
- The Blood-Labyrinth Barrier: Non-Invasive Delivery Strategies for Inner Ear Drug Delivery.Pharmaceutics · 2025Review
- A critical evaluation of "leakage" at the cochlear blood-stria-barrier and its functional significance.Frontiers in molecular neuroscience · 2024Review
- NKCC1 in human diseases: is theAmerican journal of physiology. Cell physiology · 2023Article
- Human blood-labyrinth barrier model to study the effects of cytokines and inflammation.Frontiers in molecular neuroscience · 2023Article
- Loss of NKCC1 function increases epithelial tight junction permeability by upregulating claudin-2 expression.American journal of physiology. Cell physiology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acoustic trauma, autoimmune inner ear disease, and presbycusis feature loss of the integrity of the blood-labyrinth barrier (BLB). Normal BLB function depends on endothelial structural integrity, which is supported and maintained by tight junctions and adherens junctions within the microvascular endothelial layer. When these junctions are disrupted, vascular leakage occurs. Tight junctions and adherens junctions are functionally and structurally linked, but the exact signaling pathways underlying their interaction remain unknown. In addition, solute carriers (SC) are essential for optimal exchange through BLB. Previously, we found that SC family member, the sodium-hydrogen exchanger NHE6, was expressed in all wildtype cochlear tissues, and that
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