Evidence map›Paper›PMID 26962686›Full record

ArticleCell death & disease2016

Wnt activation protects against neomycin-induced hair cell damage in the mouse cochlea.

L Liu, Y Chen, J Qi, Y Zhang, Y He, W Ni, W Li, S Zhang, S Sun, M M Taketo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. [Research progress on the protective mechanism of insulin like growth factor-1 on inner ear].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2021
    Pooled it
  2. Article
  3. Restoring Iron Homeostasis via Smoothened Inhibition: A Novel Strategy Against Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Article
  9. Rescue of cochlear vascular pathology prevents sensory hair cell loss in Norrie disease.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Review
  11. Fundamental research · 2023
    Article
  12. Article
  13. Review
  14. Review
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  19. Novel m.4268T>C mutation in the mitochondrial tRNAWorld journal of clinical cases · 2022
    Article
  20. Review

44 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 2 countries.

L LiuOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
Y ChenOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
J QiKey Laboratory for Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing, China.
Y ZhangOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
Y HeOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
W NiOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
W LiOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.ORCID http://orcid.org/0000-0002-3394-2278
S ZhangKey Laboratory for Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing, China.
S SunOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
M M TaketoDepartment of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
L WangInstitutes of Biomedical Sciences, Fudan University, Shanghai, PR China.
R ChaiKey Laboratory for Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing, China.
H LiOtorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, PR China.
National Health and Family Planning Commission · CNFudan University · CNNantong University · CNKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have reported the role of Wnt/β-catenin signaling in hair cell (HC) development, regeneration, and differentiation in the mouse cochlea; however, the role of Wnt/β-catenin signaling in HC protection remains unknown. In this study, we took advantage of transgenic mice to specifically knockout or overactivate the canonical Wnt signaling mediator β-catenin in HCs, which allowed us to investigate the role of Wnt/β-catenin signaling in protecting HCs against neomycin-induced damage. We first showed that loss of β-catenin in HCs made them more vulnerable to neomycin-induced injury, while constitutive activation of β-catenin in HCs reduced HC loss both in vivo and in vitro. We then showed that loss of β-catenin in HCs increased caspase-mediated apoptosis induced by neomycin injury, while β-catenin overexpression inhibited caspase-mediated apoptosis. Finally, we demonstrated that loss of β-catenin in HCs led to increased expression of forkhead box O3 transcription factor (Foxo3) and Bim along with decreased expression of antioxidant enzymes; thus, there were increased levels of reactive oxygen species (ROS) after neomycin treatment that might be responsible for the increased aminoglycoside sensitivity of HCs. In contrast, β-catenin overexpression reduced Foxo3 and Bim expression and ROS levels, suggesting that β-catenin is protective against neomycin-induced HC loss. Our findings demonstrate that Wnt/β-catenin signaling has an important role in protecting HCs against neomycin-induced HC loss and thus might be a new therapeutic target for the prevention of HC death.

Indexed as

AnimalsApoptosis Regulatory ProteinsBcl-2-Like Protein 11beta CateninCell DeathForkhead Box Protein O3Forkhead Transcription FactorsHair Cells, AuditoryHearing LossMembrane ProteinsMiceMice, TransgenicNeomycinProto-Oncogene ProteinsReactive Oxygen SpeciesWnt Signaling PathwayApoptosis Regulatory ProteinsBcl-2-Like Protein 11beta CateninForkhead Box Protein O3Forkhead Transcription FactorsFoxO3 protein, mouseMembrane ProteinsNeomycinProto-Oncogene ProteinsReactive Oxygen Species

Identifiers

PMID26962686
PMCPMC4823936
OpenAlexW2293889193

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.