Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (409 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The hearing and equilibrium system of the body. It consists of three parts: the external ear, the middle ear, and the inner ear. Sound waves are transmitted through this organ where vibration is transduced to nerve signals that pass through the acoustic nerve to the central nervous system. The inner ear also contains the vestibular organ that maintains equilibrium by transducing signals to the vestibular nerve.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Ears; Vestibulocochlear Apparatus; Apparatus, Vestibulocochlear; Vestibulocochlear System; System, Vestibulocochlear.
Where it fits in the MeSH classification
- Broader topics
- Head; Sense Organs
- Narrower topics
- Ear, External; Ear, Inner; Ear, Middle
Related concepts
- External Ear
- Middle Ear
- Inner Ear
- Acoustic Nerve
- Central Nervous System
- Vestibular Nerve
Research landscape
PubMed indexes 115,117 records tagged with the MeSH heading “Ear” (counts retrieved 2026-10-31). 12,815 of them (11.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 59,441 records.
Reviews account for 7,826 records (6.8%) and meta-analyses for 237. Randomized controlled trials number 1,135 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 59,441 |
| 2000-2009 | 20,000 |
| 2010-2019 | 22,861 |
| 2020 onward | 12,815 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 7,826 | 6.8% |
| Meta-analyses | 237 | 0.2% |
| Randomized controlled trials | 1,135 | 1.0% |
Method: PubMed query "Ear"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Persistence of vestibular function in the absence of glutamatergic transmission from hair cells | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41866362 · DOI · PMC13153426 |
| Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41514193 · DOI · PMC12970211 |
| Supporting cells orchestrate noise-induced hearing loss via a Gasdermin D-dependent signaling loop with hair cells | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41407982 · DOI · PMC12712061 |
Persistence of vestibular function in the absence of glutamatergic transmission from hair cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Quantal synaptic transmission in vestibular endorgans is glutamatergic.
- Closing excerpt
- We propose that non-quantal transmission is sufficient to support vestibular nerve physiology and behavioral function in Vglut3-/- mice.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Quantal synaptic transmission in vestibular endorgans is glutamatergic. Here, we investigated the vestibular phenotype of deaf Vglut3-/- (Slc17a8-/-) mice from the cellular to behavioral levels. In Vglut3-/- mice, quantal synaptic transmission in utricular calyces was reduced in rate and amplitude by > 95%. In vivo recordings of spontaneous activity in the vestibular nerve revealed no significant effect of VGLUT3 deletion on afferent rate and regularity, suggesting a divergent underlying mechanism compared to the silent Vglut3-/- auditory nerve. In behavioral studies, Vglut3-/- mice did not exhibit considerable sensorimotor or balance deficits. Type-II vestibular hair cells (VHCs) in Vglut3+/+ mice were strongly immunoreactive for VGLUT3, while type-I VHCs showed weak immunoreactivity. Collectively, these data support the view that non-quantal transmission is the predominant mode of neurotransmission between type-I VHCs and vestibular calyceal afferent neurons. We propose that non-quantal transmission is sufficient to support vestibular nerve physiology and behavioral function in Vglut3-/- mice.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41866362 · DOI · PMC13153426
Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Gap junction Beta 2 Protein (GJB2, Connexin26, Cx26), the primary genetic cause of hereditary hearing loss (25%-50% of cases), has been exclusively regarded as forming an intercellular channel that mediates rapid communication.
- Closing excerpt
- Further, we provide strategies based on mechanisms to promote the TC development and hearing rescue in Cx26 deficient cochlea, which has important implications for the discovery and development of treatment strategies for hearing loss caused by Cx26 deficiency.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (136 words)
Gap junction Beta 2 Protein (GJB2, Connexin26, Cx26), the primary genetic cause of hereditary hearing loss (25%-50% of cases), has been exclusively regarded as forming an intercellular channel that mediates rapid communication. Here, we redefine its biological role by discovering its nuclear localization and direct transcriptional regulatory function in cochlear structure development. We demonstrate that Cx26 could aggregate in the nucleus of cochlear support cell and cell lines. Cx26 can bind to the promoter transcription start point of genomic DNA and directly regulate gene transcription, thus controlling the structural development of the tunnel of Corti during cochlear development. Further, we provide strategies based on mechanisms to promote the TC development and hearing rescue in Cx26 deficient cochlea, which has important implications for the discovery and development of treatment strategies for hearing loss caused by Cx26 deficiency.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41514193 · DOI · PMC12970211
Supporting cells orchestrate noise-induced hearing loss via a Gasdermin D-dependent signaling loop with hair cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Noise-induced hearing loss (NIHL), a common sensory disorder, is traditionally thought to stem primarily from direct damage to sound-sensing hair cells (HCs).
- Closing excerpt
- Our findings uncover a central role for SCs in noise-induced hearing loss and identify GSDMD-mediated intercellular communication as a potential therapeutic target.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (123 words)
Noise-induced hearing loss (NIHL), a common sensory disorder, is traditionally thought to stem primarily from direct damage to sound-sensing hair cells (HCs). Here, we demonstrate that supporting cells (SCs), neighboring cells not previously implicated in NIHL pathogenesis, orchestrate hearing loss and HC degeneration through Gasdermin D (GSDMD) activation. Mechanistically, noise-induced oxidative stress in HCs triggers activation of epidermal growth factor receptor in SCs, leading to extracellular-regulated kinase phosphorylation and caspase-11-dependent cleavage of GSDMD, thereby establishing an HC-to-SC signaling cascade. Furthermore, GSDMD activation in SCs reciprocally exacerbates oxidative injury in HCs, creating a pathogenic positive feedback loop between the two cell types. Our findings uncover a central role for SCs in noise-induced hearing loss and identify GSDMD-mediated intercellular communication as a potential therapeutic target.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41407982 · DOI · PMC12712061
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Vestibular rehabilitation for unilateral peripheral vestibular dysfunction [4]
- Research article Endolymphatic sac surgery for Ménière's disease: a systematic review and meta-analysis [5]
- Research article Internal models of self-motion: neural computations by the vestibular cerebellum [6]
- Research article Intrinsic mechanism and pharmacologic treatments of noise-induced hearing loss [7]
- Research article A Comparison of the Effectiveness of Triamcinolone and Radiation Therapy for Ear Keloids after Surgical Excision: A Systematic Review and Meta-Analysis [8]
- Research article Comparison of endoscopic and microscopic ear surgery in pediatric patients: A meta-analysis [9]
References
- Mukhopadhyay M, Modgekar R, Yang-Hood A, Ohlemiller KK, Militchin V, Xiao M, et al.. Persistence of vestibular function in the absence of glutamatergic transmission from hair cells. . 2026. PMID 41866362 · DOI · PMC13153426
- Liu X, Xie L, Jin Y, Chen S, Shi X, Zong Y, et al.. Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development. . 2026. PMID 41514193 · DOI · PMC12970211
- Xiao L, Liu J, Chen Y, Xia L, Jiang Y, Chen X, et al.. Supporting cells orchestrate noise-induced hearing loss via a Gasdermin D-dependent signaling loop with hair cells. . 2025. PMID 41407982 · DOI · PMC12712061
- McDonnell MN, Hillier SL. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2015. PMID 25581507 · DOI · PMC11259236
- Sood AJ, Lambert PR, Nguyen SA, Meyer TA. Endolymphatic sac surgery for Ménière's disease: a systematic review and meta-analysis. Otol Neurotol. 2014. PMID 24751747 · DOI
- Cullen KE. Internal models of self-motion: neural computations by the vestibular cerebellum. Trends Neurosci. 2023. PMID 37739815 · DOI · PMC10591839
- Xu K, Xu B, Gu J, Wang X, Yu D, Chen Y. Intrinsic mechanism and pharmacologic treatments of noise-induced hearing loss. Theranostics. 2023. PMID 37441605 · DOI · PMC10334830
- Shin JY, Lee JW, Roh SG, Lee NH, Yang KM. A Comparison of the Effectiveness of Triamcinolone and Radiation Therapy for Ear Keloids after Surgical Excision: A Systematic Review and Meta-Analysis. Plast Reconstr Surg. 2016. PMID 27219228 · DOI
- Han SY, Lee DY, Chung J, Kim YH. Comparison of endoscopic and microscopic ear surgery in pediatric patients: A meta-analysis. Laryngoscope. 2019. PMID 30593662 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.