ROS-Induced Activation of DNA Damage Responses Drives Senescence-Like State in Postmitotic Cochlear Cells: Implication for Hearing Preservation.
Animals
Antioxidant Response Elements
/ genetics
Apoptosis
/ drug effects
Autophagy
/ drug effects
Cellular Senescence
/ drug effects
Cochlea
/ drug effects
DNA Damage
DNA Repair
/ drug effects
Hearing
/ physiology
Hearing Loss
/ pathology
Mice
Mitosis
/ drug effects
Organometallic Compounds
/ pharmacology
Oxidative Stress
/ drug effects
Phenotype
Reactive Oxygen Species
/ toxicity
Up-Regulation
/ drug effects
Age-related hearing loss
DNA damage responses
Hearing preservation
Oxidative stress
Senescence
Journal
Molecular neurobiology
ISSN: 1559-1182
Titre abrégé: Mol Neurobiol
Pays: United States
ID NLM: 8900963
Informations de publication
Date de publication:
Aug 2019
Aug 2019
Historique:
received:
28
08
2018
accepted:
11
01
2019
pubmed:
30
1
2019
medline:
18
12
2019
entrez:
30
1
2019
Statut:
ppublish
Résumé
In our aging society, age-related hearing loss (ARHL) has become a major socioeconomic issue. Reactive oxygen species (ROS) may be one of the main causal factors of age-related cochlear cell degeneration. We examined whether ROS-induced DNA damage response drives cochlear cell senescence and contributes to ARHL from the cellular up to the system level. Our results revealed that sublethal concentrations of hydrogen peroxide (H
Identifiants
pubmed: 30693443
doi: 10.1007/s12035-019-1493-6
pii: 10.1007/s12035-019-1493-6
pmc: PMC6614136
doi:
Substances chimiques
EUK 207
0
Organometallic Compounds
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5950-5969Subventions
Organisme : Fondation de l'Avenir pour la Recherche Médicale Appliquée
ID : Et2-675
Organisme : Fondation Gueules Cassées
ID : 25-2017 V3, 77-2017 V3
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