Redox activation of excitatory pathways in auditory neurons as mechanism of age-related hearing loss.
Age-related hearing loss
Auditory neurons
Excitotoxicity
Glutamatergic signaling
NADPH oxidase
Presbycusis
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
22
11
2019
revised:
08
01
2020
accepted:
14
01
2020
pubmed:
31
1
2020
medline:
17
4
2021
entrez:
31
1
2020
Statut:
ppublish
Résumé
Age-related hearing (ARHL) loss affects a large part of the human population with a major impact on our aging societies. Yet, underlying mechanisms are not understood, and no validated therapy or prevention exists. NADPH oxidases (NOX), are important sources of reactive oxygen species (ROS) in the cochlea and might therefore be involved in the pathogenesis of ARHL. Here we investigate ARHL in a mouse model. Wild type mice showed early loss of hearing and cochlear integrity, while animals deficient in the NOX subunit p22
Identifiants
pubmed: 32000019
pii: S2213-2317(19)31455-7
doi: 10.1016/j.redox.2020.101434
pmc: PMC7016250
pii:
doi:
Substances chimiques
Reactive Oxygen Species
0
NADPH Oxidases
EC 1.6.3.-
CYBA protein, human
EC 1.6.3.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101434Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors have declared that no conflict of interest exists.
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