Evidence map›Paper›PMID 31866822›Full record

ArticleFrontiers in molecular neuroscience2019

Transient Receptor Potential Cation Channel Subfamily Vanilloid 4 and 3 in the Inner Ear Protect Hearing in Mice.

Shengnan Wang, Qiaowei Geng, Lifang Huo, Yirui Ma, Yiting Gao, Wei Zhang, Hailin Zhang, Ping Lv, Zhanfeng Jia

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 36% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. TRP channels in mammalian hearing loss.Frontiers in molecular neuroscience · 2025
    Review
  5. Review
  6. Frontiers in pharmacology · 2024
    Article
  7. Review
  8. Cannabinoid Signaling in Auditory Function and Development.Frontiers in molecular neuroscience · 2021
    Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Shengnan WangDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Qiaowei GengDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Lifang HuoDepartment of Pharmacology, Institute of Chinese Integrative Medicine, Hebei Medical University, Shijiazhuang, China.
Yirui MaDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Yiting GaoDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Wei ZhangDepartment of Pharmacology, Institute of Chinese Integrative Medicine, Hebei Medical University, Shijiazhuang, China.
Hailin ZhangDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Ping LvDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Zhanfeng JiaDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, China.
Ministry of Education of the People's Republic of China · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transient receptor potential cation channel, vanilloid type (TRPV) 3, is a member of the TRPV subfamily that is expressed predominantly in the skin, hair follicles, and gastrointestinal tract. It is also distributed in the organ of Corti of the inner ear and colocalizes with TRPV1 or TRPV4, but its role in auditory function is unknown. In the present study, we demonstrate that TRPV3 is expressed in inner hair cells (HCs) but mainly in cochlear outer HCs in mice, with expression limited to the cytoplasm and not detected in stereocilia. We compared the number of HCs as well as distortion product otoacoustic emissions (DPOAE) and auditory brainstem response (ABR) thresholds between TRPV3 knockout (V3KO) and wild-type (V3WT) mice and found that although most mutants (72.3%) had normal hearing, a significant proportion (27.7%) showed impaired hearing associated with loss of cochlear HCs. Compensatory upregulation of TRPV4 in HCs prevented HC damage and kanamycin-induced hearing loss and preserved normal auditory function in most of these mice. Thus, TRPV4 and TRPV3 in cochlear HCs protect hearing in mice; moreover, the results suggest some functional redundancy in the functions of TRPV family members. Our findings provide novel insight into the molecular basis of auditory function in mammals that can be applied to the development of strategies to mitigate hearing loss.

Indexed as

cochlear hair cellhearingknockoutTRPVTRPV3

Identifiers

PMID31866822
PMCPMC6904345
OpenAlexW2993674193

What OpenQuestion holds

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Registered trials

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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.