Evidence map›Paper›PMID 23361190›Full record

ReviewHearing research2013

The mitochondrion: a perpetrator of acquired hearing loss.

Erik C Böttger, Jochen Schacht

Registry-linked trialAbstract readReview
In one paragraph

Review in Hearing research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06729632 (Non-Invasive System to Deliver Therapeutic Hypothermia for Protection Against Noise-Induced Hearing Loss), which is not on this map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
5.2field-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.

NCT06729632 narecruitingnot on this mapstarted 2024, after this paper: background citation

Non-Invasive System to Deliver Therapeutic Hypothermia for Protection Against Noise-Induced Hearing Loss

TypeinterventionalSponsorRestorear Devices LLCRan2024 to 2027Enrolled116ConditionsNoise Exposure, Noise-induced Hearing Loss, Noise, Adverse EffectArmsCold pack-delivered mild therapeutic hypothermia
3 · Its place in the literature

Who cites it

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. XIAP Stabilizes DDRGK1 to Promote ER-Phagy and Protects Against Noise-Induced Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. TNFAIP8L2 as a dual regulator of mTORC1 signaling: Implications for therapy in presbycusis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Electron Microscopic Mapping of Mitochondrial Morphology in the Cochlear Nerve Fibers.Journal of the Association for Research in Otolaryngology : JARO · 2024
    Article
  17. Hearing Loss and Oxidative Stress: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024
    Review
  18. Review
  19. Review
  20. Role of Oxidative Stress in Sensorineural Hearing Loss.International journal of molecular sciences · 2024
    Review

56 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

2 authors at 2 institutions in 2 countries.

Erik C BöttgerInstitut für Medizinische Mikrobiologie, Universität Zürich, Zürich, Switzerland.
Jochen Schacht
University of Michigan–Ann Arbor · USUniversity of Zurich · CH

Funding

Scientific Synergy CoreP30DC005188 · NIDCD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DOLAN, DAVID FRANCIS · 2002 to 2016
$10.3M
PROTECTION FROM AMINOGLYCOSIDE OTOTOXICITYR01DC003685 · NIDCD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCHACHT, JOCHEN · 1998 to 2013
$4.1M
NIDCD NIH HHS P30 DC005188NIDCD NIH HHS P30 DC-05188NIDCD NIH HHS R01 DC003685NIDCD NIH HHS R01 DC-03685
6 · The paper itself

Abstract

Age, drugs, and noise are major causes of acquired hearing loss. The involvement of reactive oxygen species (ROS) in hair cell death has long been discussed, but there is considerably less information available as to the mechanisms underlying ROS formation. Most cellular ROS arise in mitochondria and this review will evaluate evidence for mitochondrial pathology in general and dysfunction of the mitochondrial respiratory chain in particular in acquired hearing loss. We will discuss evidence that different pathways can lead to the generation of ROS and that oxidative stress might not necessarily be causal to all three pathologies. Finally, we will detail recent advances in exploiting knowledge of aminoglycoside-mitochondria interactions for the development of non-ototoxic antibacterials. This article is part of a Special Issue entitled "Annual Reviews 2013".

Indexed as

AminoglycosidesAnimalsCell DeathDNA, MitochondrialElectron TransportEnergy MetabolismHair Cells, AuditoryHearing LossHearing Loss, Noise-InducedHumansMitochondriaMutationPresbycusisReactive Oxygen SpeciesRNA, RibosomalAminoglycosidesDNA, MitochondrialReactive Oxygen SpeciesRNA, Ribosomalmitochondrial DNAmtDNAreactive oxygen speciesribosomal RNAROSrRNASODsuperoxide dismutase

Identifiers

PMID23361190
PMCPMC3681877
OpenAlexW1975177376

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.