Evidence map›Paper›PMID 27916698›Full record

ArticleHearing research2017

Cellular mechanisms of noise-induced hearing loss.

Arwa Kurabi, Elizabeth M Keithley, Gary D Housley, Allen F Ryan, Ann C-Y Wong

Abstract read
In one paragraph

Article in Hearing research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
195citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

195 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  11. Drug Discovery Targeting Nicotinic Acetylcholine Receptors for Hearing Loss.International journal of molecular sciences · 2026
    Review
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135 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

5 authors.

Arwa KurabiDivision of Otolaryngology, Department of Surgery, UCSD School of Medicine and San Diego VA Medical Center, La Jolla, CA, 92093, United States.
Elizabeth M KeithleyDivision of Otolaryngology, Department of Surgery, UCSD School of Medicine and San Diego VA Medical Center, La Jolla, CA, 92093, United States.
Gary D HousleyDivision of Otolaryngology, Department of Surgery, UCSD School of Medicine and San Diego VA Medical Center, La Jolla, CA, 92093, United States.
Allen F RyanDivision of Otolaryngology, Department of Surgery, UCSD School of Medicine and San Diego VA Medical Center, La Jolla, CA, 92093, United States. Electronic address: afryan@ucsd.edu.
Ann C-Y WongDivision of Otolaryngology, Department of Surgery, UCSD School of Medicine and San Diego VA Medical Center, La Jolla, CA, 92093, United States.

Funding

Basic Mechanisms on Hearing Loss of Cochlear OriginI01BX001205 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RYAN, ALLEN F. · 2013 to 2024
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A Biological Interface for Auditory Rehabilitation with a Cochlear ImplantI01RX000977 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RYAN, ALLEN F. · 2014 to 2016
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BLRD VA I01 BX001205RRD VA I01 RX000977
6 · The paper itself

Abstract

Exposure to intense sound or noise can result in purely temporary threshold shift (TTS), or leave a residual permanent threshold shift (PTS) along with alterations in growth functions of auditory nerve output. Recent research has revealed a number of mechanisms that contribute to noise-induced hearing loss (NIHL). The principle cause of NIHL is damage to cochlear hair cells and associated synaptopathy. Contributions to TTS include reversible damage to hair cell (HC) stereocilia or synapses, while moderate TTS reflects protective purinergic hearing adaptation. PTS represents permanent damage to or loss of HCs and synapses. While the substrates of HC damage are complex, they include the accumulation of reactive oxygen species and the active stimulation of intracellular stress pathways, leading to programmed and/or necrotic cell death. Permanent damage to cochlear neurons can also contribute to the effects of NIHL, in addition to HC damage. These mechanisms have translational potential for pharmacological intervention and provide multiple opportunities to prevent HC damage or to rescue HCs and spiral ganglion neurons that have suffered injury. This paper reviews advances in our understanding of cellular mechanisms that contribute to NIHL and their potential for therapeutic manipulation.

Indexed as

HearingAnimalsApoptosisAuditory FatigueCalcium SignalingHair Cells, AuditoryHearing Loss, Noise-InducedHumansNecrosisNoiseOxidative StressApoptosisDamage signalingHair cellNoise-induced hearing lossPharmacotherapySurvival signaling

Identifiers

PMID27916698
PMCPMC6750278

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.