ReviewAntioxidants & redox signaling2009
Gap-junction channels dysfunction in deafness and hearing loss.
Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 167 citations in OpenAlex.
- Article
- Association of GJB2 P.V37I With Sudden Sensorineural Hearing Loss and Endoplasmic Reticulum Stress.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2026Article
- Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026Review
- Cochlear Homeostasis in Sensorineural Hearing Loss: Mechanisms, Implications, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Connexins in Acquired Hearing Loss: Expanding Research Perspectives.Biomedicines · 2025Review
- Transcriptomic and metabolomic basis of seasonal auditory sensitivity variations in the red-eared slider (Trachemys scripta elegans).BMC genomics · 2025Article
- Anatomical and molecular insights into avian inner ear sensory hair cell regeneration.Developmental biology · 2025Review
- Distinct Connexin43, Connexin31, and Pannexin1 expression patterns in the cochlea of a non-human primate.Scientific reports · 2025Article
- Calcium Regulation of Connexin Hemichannels.International journal of molecular sciences · 2024Review
- Comparison of vestibular function in hereditary hearing loss patients with GJB2, CDH23, and SLC26A4 variants.Scientific reports · 2024Article
- Connexins 30 and 43 expression changes in relation to age-related hearing loss.Hearing research · 2024Article
- Identification of common stria vascularis cellular alteration in sensorineural hearing loss based on ScRNA-seq.BMC genomics · 2024Article
- Identification and validation of a gap junction protein related signature for predicting the prognosis of renal clear cell carcinoma.Frontiers in oncology · 2024Article
- Gene therapy for hearing loss: challenges and the promise of cellular plasticity and epigenetic modulation.Frontiers in neurology · 2024Article
- Functional Consequences of Pathogenic Variants of theBiomolecules · 2023Review
- Advances in gene therapy hold promise for treating hereditary hearing loss.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Molecular Mechanisms and Clinical Phenotypes ofBiology · 2023Review
- A Connexin Gene (Frontiers in genetics · 2022Article
- Expression of KID syndromic mutation Cx26S17F produces hyperactive hemichannels in supporting cells of the organ of Corti.Frontiers in cell and developmental biology · 2022Article
- Connexin 30 deletion exacerbates cochlear senescence and age-related hearing loss.Frontiers in cell and developmental biology · 2022Article
21 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
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Gap-junction channels connect the cytoplasm of adjacent cells, allowing the diffusion of ions and small metabolites. They are formed at the appositional plasma membranes by a family of related proteins named connexins. Mutations in connexins 26, 31, 30, 32, and 43 have been associated with nonsyndromic or syndromic deafness. The majority of these mutations are inherited in an autosomal recessive manner, but a few of them have been associated with dominantly inherited hearing loss. Mutations in the connexin26 gene (GJB2) are the most common cause of genetic deafness. This review summarizes the most relevant and recent information about different mutations in connexin genes found in human patients, with emphasis on GJB2. The possible effects of the mutations on channel expression and function are discussed, in addition to their possible physiologic consequences for inner ear physiology. Finally, we propose that connexin channels (gap junctions and hemichannels) may be targets for age-related hearing loss induced by oxidative damage.
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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.