Evidence map›Paper›PMID 31379853›Full record

ArticleFrontiers in immunology2019

Nfatc4 Deficiency Attenuates Ototoxicity by Suppressing Tnf-Mediated Hair Cell Apoptosis in the Mouse Cochlea.

Yanping Zhang, Diyan Chen, Liping Zhao, Wen Li, Yusu Ni, Yan Chen, Huawei Li

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

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Yanping ZhangState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Diyan ChenState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Liping ZhaoState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Wen LiState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Yusu NiState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Yan ChenState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Huawei LiState Key Laboratory of Medical Neurobiology, Department of Affiliated Eye and ENT Hospital, ENT Institute and Otorhinolaryngology, Institutes of Biomedical Sciences and the Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Eye & ENT Hospital of Fudan University · CNFudan University · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The loss of sensory hair cells in the cochlea is the major cause of sensorineural hearing loss, and inflammatory processes and immune factors in response to cochlear damage have been shown to induce hair cell apoptosis. The expression and function of Nfatc4 in the cochlea remains unclear. In this study, we investigated the expression of Nfatc4 in the mouse cochlea and explored its function using

Indexed as

AnimalsApoptosisCell NucleusCochleaCytoplasmHair Cells, AuditoryHearing LossInflammationMiceMice, KnockoutNFATC Transcription FactorsOtotoxicityNfatc4 protein, mouseNFATC Transcription Factorscell apoptosiscochlear hair cellshearing lossinflammationinner earNfatc4

Identifiers

PMID31379853
PMCPMC6650568
OpenAlexW2959522768

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.