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: 4 complete abstracts (716 words), 10 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 part of the inner ear (labyrinth) that is concerned with hearing. It forms the anterior part of the labyrinth, as a snail-like structure that is situated almost horizontally anterior to the vestibular labyrinth.
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: Cochleas.
Where it fits in the MeSH classification
- Broader topics
- Ear, Inner
- Narrower topics
- Basilar Membrane; Cochlear Aqueduct; Cochlear Duct; Organ of Corti; Round Window, Ear; Scala Tympani; Scala Vestibuli; Spiral Ganglion; Spiral Lamina; Spiral Ligament of Cochlea
- See also
- Otoacoustic Emissions, Spontaneous
Related concepts
- Labyrinth
- Vestibular Labyrinth
Research landscape
PubMed indexes 31,776 records tagged with the MeSH heading “Cochlea” (counts retrieved 2026-10-31). 4,123 of them (13.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 14,398 records.
Reviews account for 2,152 records (6.8%) and meta-analyses for 26. Randomized controlled trials number 71 (0.2%) 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 | 14,398 |
| 2000-2009 | 6,347 |
| 2010-2019 | 6,908 |
| 2020 onward | 4,123 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,152 | 6.8% |
| Meta-analyses | 26 | 0.1% |
| Randomized controlled trials | 71 | 0.2% |
Method: PubMed query "Cochlea"[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 |
|---|---|---|---|---|
| FOXO1-NCOA4 Axis Contributes to Cisplatin-Induced Cochlea Spiral Ganglion Neuron Ferroptosis via Ferritinophagy | 2024 | Research article Design not recorded in structured metadata | 31 | cc by PMID 39206719 · DOI · PMC11515924 |
| Complexes of vertebrate TMC1/2 and CIB2/3 proteins form hair-cell mechanotransduction cation channels | 2025 | Research article Design not recorded in structured metadata | 24 | cc0 PMID 39773557 · DOI · PMC11709434 |
| Deciphering Compromised Speech-in-Noise Intelligibility in Older Listeners: The Role of Cochlear Synaptopathy | 2025 | Research article Design not recorded in structured metadata | 23 | cc by PMID 39788732 · DOI · PMC11842038 |
| 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 |
FOXO1-NCOA4 Axis Contributes to Cisplatin-Induced Cochlea Spiral Ganglion Neuron Ferroptosis via Ferritinophagy [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mammalian cochlea spiral ganglion neurons (SGNs) are crucial for sound transmission, they can be damaged by chemotherapy drug cisplatin and lead to irreversible sensorineural hearing loss (SNHL), while such damage can also render cochlear implants ineffective.
- Closing excerpt
- Collectively, this study highlights the critical role of the FOXO1-NCOA4 axis in regulating ferritinophagy and ferroptosis in cisplatin-induced SGNs damage, offering promising therapeutic targets for SNHL mitigation.
- 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 (194 words)
Mammalian cochlea spiral ganglion neurons (SGNs) are crucial for sound transmission, they can be damaged by chemotherapy drug cisplatin and lead to irreversible sensorineural hearing loss (SNHL), while such damage can also render cochlear implants ineffective. However, the mechanisms underlying cisplatin-induced SGNs damage and subsequent SNHL are still under debate and there is no currently effective clinical treatment. Here, this study demonstrates that ferroptosis is triggered in SGNs following exposure to cisplatin. Inhibiting ferroptosis protects against cisplatin-induced SGNs damage and hearing loss, while inducing ferroptosis intensifies these effects. Furthermore, cisplatin prompts nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy in SGNs, while knocking down NCOA4 mitigates cisplatin-induced ferroptosis and hearing loss. Notably, the upstream regulator of NCOA4 is identified and transcription factor forkhead box O1 (FOXO1) is shown to directly suppress NCOA4 expression in SGNs. The knocking down of FOXO1 amplifies NCOA4-mediated ferritinophagy, increases ferroptosis and lipid peroxidation, while disrupting the interaction between FOXO1 and NCOA4 in NCOA4 knock out mice prevents the cisplatin-induced SGN ferroptosis and hearing loss. Collectively, this study highlights the critical role of the FOXO1-NCOA4 axis in regulating ferritinophagy and ferroptosis in cisplatin-induced SGNs damage, offering promising therapeutic targets for SNHL mitigation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39206719 · DOI · PMC11515924
Complexes of vertebrate TMC1/2 and CIB2/3 proteins form hair-cell mechanotransduction cation channels [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Calcium and integrin-binding protein 2 (CIB2) and CIB3 bind to transmembrane channel-like 1 (TMC1) and TMC2, the pore-forming subunits of the inner-ear mechano-electrical transduction (MET) apparatus.
- Closing excerpt
- Overall, our work demonstrates that intact CIB2/3 and TMC1/2 complexes are integral to hair-cell MET function in vertebrate mechanosensory epithelia.
- 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 (158 words)
Calcium and integrin-binding protein 2 (CIB2) and CIB3 bind to transmembrane channel-like 1 (TMC1) and TMC2, the pore-forming subunits of the inner-ear mechano-electrical transduction (MET) apparatus. These interactions have been proposed to be functionally relevant across mechanosensory organs and vertebrate species. Here, we show that both CIB2 and CIB3 can form heteromeric complexes with TMC1 and TMC2 and are integral for MET function in mouse cochlea and vestibular end organs as well as in zebrafish inner ear and lateral line. Our AlphaFold 2 models suggest that vertebrate CIB proteins can simultaneously interact with at least two cytoplasmic domains of TMC1 and TMC2 as validated using nuclear magnetic resonance spectroscopy of TMC1 fragments interacting with CIB2 and CIB3. Molecular dynamics simulations of TMC1/2 complexes with CIB2/3 predict that TMCs are structurally stabilized by CIB proteins to form cation channels. Overall, our work demonstrates that intact CIB2/3 and TMC1/2 complexes are integral to hair-cell MET function in vertebrate mechanosensory epithelia.
Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 39773557 · DOI · PMC11709434
Deciphering Compromised Speech-in-Noise Intelligibility in Older Listeners: The Role of Cochlear Synaptopathy [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Speech intelligibility declines with age and sensorineural hearing damage (SNHL).
- Closing excerpt
- We conclude that age-related CS reduces supra-threshold temporal envelope coding with subsequent speech coding deficits in noise that cannot be explained based on hearing sensitivity alone.
- 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 (228 words)
Speech intelligibility declines with age and sensorineural hearing damage (SNHL). However, it remains unclear whether cochlear synaptopathy (CS), a recently discovered form of SNHL, significantly contributes to this issue. CS refers to damaged auditory-nerve synapses that innervate the inner hair cells and there is currently no go-to diagnostic test available. Furthermore, age-related hearing damage can comprise various aspects (e.g., hair cell damage, CS) that each can play a role in impaired sound perception. To explore the link between cochlear damage and speech intelligibility deficits, this study examines the role of CS for word recognition among older listeners. We first validated an envelope-following response (EFR) marker for CS using a Budgerigar model. We then applied this marker in human experiments, while restricting the speech material's frequency content to ensure that both the EFR and the behavioral tasks engaged similar cochlear frequency regions. Following this approach, we identified the relative contribution of hearing sensitivity and CS to speech intelligibility in two age-matched (65-year-old) groups with clinically normal (n = 15, 8 females) or impaired audiograms (n = 13, 8 females). Compared to a young normal-hearing control group (n = 13, 7 females), the older groups demonstrated lower EFR responses and impaired speech reception thresholds. We conclude that age-related CS reduces supra-threshold temporal envelope coding with subsequent speech coding deficits in noise that cannot be explained based on hearing sensitivity alone.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39788732 · DOI · PMC11842038
Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development [4]
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
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 Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms [5]
- Research article Hair Cell Transduction, Tuning, and Synaptic Transmission in the Mammalian Cochlea [6]
- Research article Integrating the active process of hair cells with cochlear function [7]
- Research article Pathology and mechanisms of cochlear aging [8]
- Research article The search for noise-induced cochlear synaptopathy in humans: Mission impossible? [9]
- Research article Sensory Processing at Ribbon Synapses in the Retina and the Cochlea [10]
References
- Wang X, Xu L, Meng Y, Chen F, Zhuang J, Wang M, et al.. FOXO1-NCOA4 Axis Contributes to Cisplatin-Induced Cochlea Spiral Ganglion Neuron Ferroptosis via Ferritinophagy. . 2024. PMID 39206719 · DOI · PMC11515924
- Giese APJ, Weng WH, Kindt KS, Chang HHV, Montgomery JS, Ratzan EM, et al.. Complexes of vertebrate TMC1/2 and CIB2/3 proteins form hair-cell mechanotransduction cation channels. . 2025. PMID 39773557 · DOI · PMC11709434
- Garrett M, Vasilkov V, Mauermann M, Devolder P, Wilson JL, Gonzales L, et al.. Deciphering Compromised Speech-in-Noise Intelligibility in Older Listeners: The Role of Cochlear Synaptopathy. . 2025. PMID 39788732 · DOI · PMC11842038
- 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
- Liberman MC, Kujawa SG. Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms. Hear Res. 2017. PMID 28087419 · DOI · PMC5438769
- Fettiplace R. Hair Cell Transduction, Tuning, and Synaptic Transmission in the Mammalian Cochlea. Compr Physiol. 2017. PMID 28915323 · DOI · PMC5658794
- Hudspeth AJ. Integrating the active process of hair cells with cochlear function. Nat Rev Neurosci. 2014. PMID 25096182 · DOI
- Keithley EM. Pathology and mechanisms of cochlear aging. J Neurosci Res. 2020. PMID 31066107 · DOI · PMC7496655
- Bramhall N, Beach EF, Epp B, Le Prell CG, Lopez-Poveda EA, Plack CJ, et al.. The search for noise-induced cochlear synaptopathy in humans: Mission impossible?. Hear Res. 2019. PMID 30921644 · DOI
- Moser T, Grabner CP, Schmitz F. Sensory Processing at Ribbon Synapses in the Retina and the Cochlea. Physiol Rev. 2020. PMID 31373863 · 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.