ArticleAging2019
Down-regulation of Cav1.3 in auditory pathway promotes age-related hearing loss by enhancing calcium-mediated oxidative stress in male mice.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
- Multitarget protection by Chinese herbal medicines against sensorineural hearing loss: a focus on oxidative stress, apoptosis, and inflammation.Frontiers in medicine · 2026Review
- Sodium hexachloroplatinate (IV) induces concentration- and time-dependent depolarization and cytotoxicity in HEI-OC1 auditory cells.PloS one · 2026Article
- AIMP1 exerts hearing protection role in age related hearing loss mice by regulating SIRT1 expression.BMC geriatrics · 2025Article
- Article
- Expression Patterns of Cav1.3 in the Developing Stria Vascularis of Sprague-Dawley Rats.The journal of international advanced otology · 2025Article
- Age-related hearing loss and its potential drug candidates: a systematic review.Chinese medicine · 2023Review
- Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss.Clinical and experimental otorhinolaryngology · 2023Article
- Current Advances in Gene Therapies of Genetic Auditory Neuropathy Spectrum Disorder.Journal of clinical medicine · 2023Review
- Current Advances in Adeno-Associated Virus-Mediated Gene Therapy to Prevent Acquired Hearing Loss.Journal of the Association for Research in Otolaryngology : JARO · 2022Review
- LncRNA H19 inhibits oxidative stress injury of cochlear hair cells by regulating miR-653-5p/SIRT1 axis.Acta biochimica et biophysica Sinica · 2022Article
- Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model.Current medical science · 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
- Auditory Neuropathy Spectrum Disorders: From Diagnosis to Treatment: Literature Review and Case Reports.Journal of clinical medicine · 2020Review
- Protection of Cochlear Ribbon Synapses and Prevention of Hidden Hearing Loss.Neural plasticity · 2020Review
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
In this study, age related Cav1.3 expression in cochlea and auditory cortex of C57BL/6J male mice was evaluated. It was found that the expression of Cav1.3 in cochlea decreased with aging whereas this phenomenon was not observed in neuron of auditory cortex. The correlation between decreased expression of Cav1.3 and age-related hearing losses was studied in vitro, after Cav1.3 was knocked out, the rate of apoptosis of hair cells increased after being subjected to ROS stresses, accompanied with enhanced senescence. Further, Cav1.3 knock down also interfered with the electrophysiology of hair cells. The effect was further confirmed in vivo, after Cav1.3 knocked down by injection of AAV, hearing impairment was observed in C57BL/6J male mice subjected to senescence and this was accompanied by increased loss of hair cells in cochlea. The effect was further confirmed in 3D organ culture, increased loss of hair cells after Cav1.3 was knocked down under ROS stresses.Mechanistically, Cav1.3 knock out resulted in decreased intracellular calcium which subsequently reduced the inactivation of ROS from complex I, and finally resulted in increased intracellular ROS and enhanced senescence.Collectively, these findings confirmed that Cav1.3 could protect cells in auditory pathway from oxidative stresses, and decreased expression of Cav1.3 in auditory pathway could contribute to hearing losses by enhancement of calcium-mediated oxidative stress.
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