ReviewCell and tissue research2015
Connexins and gap junctions in the inner ear--it's not just about K⁺ recycling.
Review in Cell and tissue research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 108 citations in OpenAlex.
- Genotype-guided Recall Delineates the Adult Auditory Phenotype in GJB2 p.V37I Homozygotes: High-frequency Vulnerability and Environmental Modulation.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2026Article
- Spontaneous Calcium Signalling in the Developing Mammalian Cochlea.Journal of the Association for Research in Otolaryngology : JARO · 2026Review
- Connexin 26 in Hearing Health and Disease: StructuralFoundations, Mutation Mechanisms, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026Review
- Spontaneous CaExperimental physiology · 2026Article
- GJB2 c.109G > A mutation activating IFI27-mediated mitochondrial apoptosis pathway leading to hereditary non-syndromic hearing loss.Scientific reports · 2026Article
- Cochlear Homeostasis in Sensorineural Hearing Loss: Mechanisms, Implications, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Insights Into Stria Vascular Function, Stria Immunity, and Age-Related Hearing Loss.Journal of the Association for Research in Otolaryngology : JARO · 2025Review
- Direct connexin-26 interactions with membrane proteins functionally relevant to the cochlea.Human genetics · 2025Article
- Distinct Connexin43, Connexin31, and Pannexin1 expression patterns in the cochlea of a non-human primate.Scientific reports · 2025Article
- In vivo spontaneous CaNature communications · 2025Article
- Common genetic etiologies of sensorineural hearing loss in Koreans.Genomics & informatics · 2024Review
- Genetic Basis of Hearing Loss in Mongolian Patients: A Next-Generation Sequencing Study.Genes · 2024Article
- Optogenetics Reveals Roles for Supporting Cells in Force Transmission to and From Outer Hair Cells in the Mouse Cochlea.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Simultaneous recordings from vestibular Type I hair cells and their calyceal afferents in mice.Frontiers in neurology · 2024Article
- Age-related changes in P2Y receptor signalling in mouse cochlear supporting cells.The Journal of physiology · 2023Article
- CaInternational journal of molecular sciences · 2023Article
- Preservation of developmental spontaneous activity enables early auditory system maturation in deaf mice.PLoS biology · 2023Article
- The applications of CRISPR/Cas-mediated genome editing in genetic hearing loss.Cell & bioscience · 2023Review
- The pathogenesis of common Gjb2 mutations associated with human hereditary deafness in mice.Cellular and molecular life sciences : CMLS · 2023Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Normal development, function and repair of the sensory epithelia in the inner ear are all dependent on gap junctional intercellular communication. Mutations in the connexin genes GJB2 and GJB6 (encoding CX26 and CX30) result in syndromic and non-syndromic deafness via various mechanisms. Clinical vestibular defects, however, are harder to connect with connexin dysfunction. Cx26 and Cx30 proteins are widely expressed in the epithelial and connective tissues of the cochlea, where they may form homomeric or heteromeric gap junction channels in a cell-specific and spatiotemporally complex fashion. Despite the study of mutant channels and animal models for both recessive and dominant autosomal deafness, it is still unclear why gap junctions are essential for auditory function, and why Cx26 and Cx30 do not compensate for each other in vivo. Cx26 appears to be essential for normal development of the auditory sensory epithelium, but may be dispensable during normal hearing. Cx30 appears to be essential for normal repair following sensory cell loss. The specific modes of intercellular signalling mediated by inner ear gap junction channels remain undetermined, but they are hypothesised to play essential roles in the maintenance of ionic and metabolic homeostasis in the inner ear. Recent studies have highlighted involvement of gap junctions in the transfer of essential second messengers between the non-sensory cells, and have proposed roles for hemichannels in normal hearing. Here, we summarise the current knowledge about the molecular and functional properties of inner ear gap junctions, and about tissue pathologies associated with connexin mutations.
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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.