ArticleOncotarget2015
Autophagy through 4EBP1 and AMPK regulates oxidative stress-induced premature senescence in auditory cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- SIRT1 activation by SRT2104 enhances mitophagy and reduces senescence in auditory cells.Scientific reports · 2026Article
- Melatonin Ameliorates Senescence of Mouse Auditory Cell Line HEI-OC1 Cells by Suppressing NLRP3 Inflammasome-Mediated Pyroptosis.Molecular neurobiology · 2025Article
- Autophagy Induction by Mangiferin Protects Auditory Hair Cells from Ototoxicity.Molecular neurobiology · 2025Article
- The differential expression profiles of miRNA in serum-derived exosomes and its potential role in age-related hearing loss.Frontiers in aging neuroscience · 2025Article
- The Role of Molecular and Cellular Aging Pathways on Age-Related Hearing Loss.International journal of molecular sciences · 2024Review
- Premature senescence is regulated by crosstalk among TFEB, the autophagy lysosomal pathway and ROS derived from damaged mitochondria in NaAsOCell death discovery · 2024Article
- Preventive Effect of Cocoa Flavonoids via Suppression of Oxidative Stress-Induced Apoptosis in Auditory Senescent Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Elucidation of the mechanism of miR-122-5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide.Experimental and therapeutic medicine · 2022Article
- Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Urolithin A attenuates auditory cell senescence by activating mitophagy.Scientific reports · 2022Article
- Pyrroloquinoline quinone (PQQ) protects mitochondrial function of HEI-OC1 cells under premature senescence.npj aging · 2022Article
- Cellular autophagy, the compelling roles in hearing function and dysfunction.Frontiers in cellular neuroscience · 2022Review
- Role of Oxidative Stress in the Senescence Pattern of Auditory Cells in Age-Related Hearing Loss.Antioxidants (Basel, Switzerland) · 2021Article
- Prediction of the Molecular Mechanisms Underlying Erlong Zuoci Treatment of Age-Related Hearing Loss via Network Pharmacology-Based Analyses Combined with Experimental Validation.Frontiers in pharmacology · 2021Article
- Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis.Cell proliferation · 2020Review
- Article
- Comprehensive Map of the Regulated Cell Death Signaling Network: A Powerful Analytical Tool for Studying Diseases.Cancers · 2020Article
- Implications of Oxidative Stress and Cellular Senescence in Age-Related Thymus Involution.Oxidative medicine and cellular longevity · 2020Review
- Integrating cellular senescence with the concept of damage accumulation in aging: Relevance for clearance of senescent cells.Aging cell · 2019Review
- Ectopic localization of autophagosome in fatty liver is a key factor for liver regeneration.Organogenesis · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to determine whether autophagy and AMPK contribute to premature senescence in auditory cells. Incubating HEI-OC1 auditory cells with 5 mM H2O2 for 1 h induced senescence, as demonstrated by senescence-associated β-galactosidase (SA-β-gal) staining. H2O2 treatment significantly delayed population-doubling time, leaving cell viability unchanged. Furthermore, the proportion of SA-β-gal-positive cells significantly increased. Autophagy-related protein expression increased, with Atg7 and LC3-II peaking 6 h and Lamp2 peaking 24 h after H2O2 treatment. The expression of these proteins decreased 48 h after treatment. Transmission electron microscopy revealed lipofuscin and aggregates within autolysosomes, which accumulated markedly in the cytoplasm of HEI-OC1 cells 48 h after treatment. Akt and P70S6 phosphorylation markedly decreased after H2O2 treatment, but 4EBP1 phosphorylation significantly increased 48 h after treatment. After RNAi-mediated knockdown (KD) of Atg7 and AMPK, H2O2-treated cells displayed dense SA-β-gal staining. Also, premature senescence was significantly induced. These suggest that a negative feedback loop may exist between autophagy and AMPK signaling pathways in HEI-OC1 cells. In our model, oxidative stress-induced premature senescence occurred due to impaired autophagy function through 4EBP1 phosphorylation. Our results also indicate that AMPK may regulate premature senescence in auditory cells in an autophagy-dependent and independent manner.
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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.