ArticleCell death & disease2017
Activation of miR-34a impairs autophagic flux and promotes cochlear cell death via repressing ATG9A: implications for age-related hearing loss.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 75 citations in OpenAlex.
- MiR-182 and MiR-34a regulate autophagy and apoptosis in tuberculosis and lung cancer.Molecular biology reports · 2026Article
- Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026Review
- Advances in the treatment of age-related hearing loss: from molecular mechanisms to targeted interventions.Frontiers in aging neuroscience · 2026Review
- Progress on multifunctional transmembrane protein ATG9A.Cell communication and signaling : CCS · 2025Review
- miR‑34a induces apoptosis and pyroptosis in D‑Galactose‑induced aging cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunctionInternational journal of molecular medicine · 2025Article
- Conditional Overexpression of Neuritin in Supporting Cell Protects Cochlear Hair Cell and Delays Age-Related Hearing Loss by Enhancing Autophagy.International journal of molecular sciences · 2025Article
- Review
- Pathophysiological insights and therapeutic developments in age-related hearing loss: a narrative review.Frontiers in aging neuroscience · 2025Review
- Beyond the auditory system: cognitive implications of age-related hearing loss.Frontiers in aging neuroscience · 2025Review
- The differential expression profiles of miRNA in serum-derived exosomes and its potential role in age-related hearing loss.Frontiers in aging neuroscience · 2025Article
- Differential expression and regulation of FASLG by miR-5195/miR-3941 in age-related hearing loss.PloS one · 2025Article
- Bile Acid Application in Cell-Targeting for Molecular Receptors in Relation to Hearing: A Comprehensive Review.Current drug targets · 2024Review
- Abnormal Cholesterol Metabolism and Lysosomal Dysfunction Induce Age-Related Hearing Loss by Inhibiting mTORC1-TFEB-Dependent Autophagy.International journal of molecular sciences · 2023Article
- Review
- ATG9A modulated by miR-195-5p can boost the malignant progression of cervical cancer cells.Epigenetics · 2023Article
- The cochlea is built to last a lifetime.Hearing research · 2023Review
- CRISPR/Cas9-mediated inactivation of miR-34a and miR-34b/c in HCT116 colorectal cancer cells: comprehensive characterization after exposure to 5-FU reveals EMT and autophagy as key processes regulated by miR-34.Cell death and differentiation · 2023Article
- miR-34a/DRP-1-mediated mitophagy participated in cisplatin-induced ototoxicity via increasing oxidative stress.BMC pharmacology & toxicology · 2023Article
- Article
- NcRNA: key and potential in hearing loss.Frontiers in neuroscience · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related hearing loss is a major unresolved public health problem. We have previously elucidated that the activation of cochlear miR-34a is correlated with age-related hearing loss in C57BL/6 mice. A growing body of evidence points that aberrant autophagy promotes cell death during the development of multiple age-related diseases. The aim of this study was to investigate the role of miR-34a-involved disorder of autophagy in the pathogenesis of age-related hearing loss. Our results showed that miR-34a expression was markedly upregulated in the aging cochlea accompanied with impairment of autophagic flux. In the inner ear HEI-OC1 cell line, miR-34a overexpression resulted in an accumulation of phagophores and impaired autophagosome-lysosome fusion, and led to cell death subsequently. Notably, autophagy-related protein 9A (ATG9A), an autophagy protein, was significantly decreased after miR-34a overexpression. Knockdown of ATG9A inhibited autophagy flux, which is similar to the effects of miR-34a overexpression. Moreover, ursodeoxycholic acid significantly rescued miR-34a-induced HEI-OC1 cell death by restoring autophagy activity. Collectively, these findings increase our understanding of the biological effects of miR-34a in the development of age-related hearing loss and highlight miR-34a as a promising therapeutic target for its treatment.
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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.