Evidence map›Paper›PMID 34843580›Full record

ArticlePloS one2021

Virus-infection in cochlear supporting cells induces audiosensory receptor hair cell death by TRAIL-induced necroptosis.

Yushi Hayashi, Hidenori Suzuki, Wataru Nakajima, Ikuno Uehara, Atsuko Tanimura, Toshiki Himeda, Satoshi Koike, Tatsuya Katsuno, Shin-Ichiro Kitajiri, Naoto Koyanagi and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Advances in the study of death receptor 5.Frontiers in pharmacology · 2025
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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

16 authors at 6 institutions in 1 country.

Yushi HayashiDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Hidenori SuzukiDivision of Morphological and Biomolecular Research, Nippon Medical School, Tokyo, Japan.
Wataru NakajimaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Ikuno UeharaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Atsuko TanimuraDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Toshiki HimedaDepartment of Microbiology, Kanazawa Medical University School of Medicine, Ishikawa, Japan.
Satoshi KoikeNeurovirology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Tatsuya KatsunoDepartment of Otolaryngology, Head and Neck Surgery, Kyoto University, Kyoto, Japan.
Shin-Ichiro KitajiriDepartment of Otolaryngology, Head and Neck Surgery, Kyoto University, Kyoto, Japan.
Naoto KoyanagiDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yasushi KawaguchiDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Koji OnomotoDivision of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Hiroki KatoLaboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Mitsutoshi YoneyamaDivision of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Takashi FujitaLaboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Nobuyuki TanakaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.ORCID 0000-0002-6373-2220
Nippon Medical School · JPKyoto University · JPChiba University · JPThe University of Tokyo · JPKanazawa Medical University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although sensorineural hearing loss (SHL) is relatively common, its cause has not been identified in most cases. Previous studies have suggested that viral infection is a major cause of SHL, especially sudden SHL, but the system that protects against pathogens in the inner ear, which is isolated by the blood-labyrinthine barrier, remains poorly understood. We recently showed that, as audiosensory receptor cells, cochlear hair cells (HCs) are protected by surrounding accessory supporting cells (SCs) and greater epithelial ridge (GER or Kölliker's organ) cells (GERCs) against viral infections. Here, we found that virus-infected SCs and GERCs induce HC death via production of the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). Notably, the HCs expressed the TRAIL death receptors (DR) DR4 and DR5, and virus-induced HC death was suppressed by TRAIL-neutralizing antibodies. TRAIL-induced HC death was not caused by apoptosis, and was inhibited by necroptosis inhibitors. Moreover, corticosteroids, the only effective drug for SHL, inhibited the virus-induced transformation of SCs and GERCs into macrophage-like cells and HC death, while macrophage depletion also inhibited virus-induced HC death. These results reveal a novel mechanism underlying virus-induced HC death in the cochlear sensory epithelium and suggest a possible target for preventing virus-induced SHL.

Indexed as

NecroptosisAnimalsCells, CulturedHair Cells, AuditoryHearing Loss, SensorineuralMiceMice, Inbred ICRTNF-Related Apoptosis-Inducing LigandVirus DiseasesTNF-Related Apoptosis-Inducing LigandTnfsf10 protein, mouse

Identifiers

PMID34843580
PMCPMC8629241
OpenAlexW3215603641

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.