Evidence map›Paper›PMID 37178259›Full record

ArticleCellular and molecular life sciences : CMLS2023

The pathogenesis of common Gjb2 mutations associated with human hereditary deafness in mice.

Qing Li, Chong Cui, Rongyu Liao, Xidi Yin, Daqi Wang, Yanbo Cheng, Bowei Huang, Liqin Wang, Meng Yan, Jinan Zhou and 8 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026
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  7. Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Treating Hearing Loss: From Cochlear Implantation to Gene Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  12. Combined AAV-mediated specific Gjb2 expression restores hearing in DFNB1 mouse models.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. AAV-mediated Gene Therapy for Hereditary Deafness: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  17. Review
  18. 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

18 authors at 4 institutions in 1 country.

Qing Li *State Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China. liqing2015@sibcb.ac.cn.ORCID http://orcid.org/0000-0002-6392-9699
Chong Cui *ENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Rongyu Liao *State Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Xidi Yin *State Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Daqi Wang *ENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Yanbo ChengSchool of Life Science and Technology, Shanghai Tech University, Shanghai, China.
Bowei HuangENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Liqin WangENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Meng YanSchool of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, China.
Jinan ZhouENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Jingjing ZhaoENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Wei TangState Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Yingyi WangSchool of Life Science and Technology, Shanghai Tech University, Shanghai, China.
Xiaohan WangRenerval Biotherapeutics, Jiangsu, China.
Jun LvENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
Jinsong LiState Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Huawei LiENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China. hwli@shmu.edu.cn.
Yilai ShuENT Institute and Department of Otorhinolaryngology, Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China. yilai_shu@fudan.edu.cn.
Fudan University · CNChinese Academy of Sciences · CNShanghaiTech University · CNUniversity of Chinese Academy of Sciences · CN

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 3210060158National Natural Science Foundation of China 82171148National Natural Science Foundation of China 82225014the National Key R&D Program of China 2020YFA0908201
6 · The paper itself

Abstract

Mutations in GJB2 (Gap junction protein beta 2) are the most common genetic cause of non-syndromic hereditary deafness in humans, especially the 35delG and 235delC mutations. Owing to the homozygous lethality of Gjb2 mutations in mice, there are currently no perfect mouse models carrying Gjb2 mutations derived from patients for mimicking human hereditary deafness and for unveiling the pathogenesis of the disease. Here, we successfully constructed heterozygous Gjb2

Indexed as

DeafnessHearing Loss, SensorineuralAnimalsConnexin 26ConnexinsHearingHumansMiceMutationConnexin 26ConnexinsGjb2 protein, mouse235delC35delGCX26CX30Gap junction channelsHair cell developmentHearing loss

Identifiers

PMID37178259
PMCPMC10182940
OpenAlexW4376504008

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.