ArticleInternational journal of molecular sciences2020
Mitochondrial Damage and Necroptosis in Aging Cochlea.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- Decoding the renal-cochlear axis: explainable machine learning and phenotype clustering reveal high-risk hearing loss subtypes in CKD.Renal failure · 2026Article
- Genomic and Epigenomic Advances in Hearing Loss: Molecular Mechanisms, Diagnostics, and Emerging Therapies.Journal of personalized medicine · 2026Review
- Precision Diagnostics in Age-Related Hearing Loss: Emerging Molecular Biomarkers for Early Detection and Targeted Prevention.International journal of general medicine · 2026Review
- Connexins in Acquired Hearing Loss: Expanding Research Perspectives.Biomedicines · 2025Review
- Targeting Ferroptosis in Sensorineural Hearing Loss: A Mechanistic Review of Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Presbycusis: Pathology, Signal Pathways, and Therapeutic Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Review
- Targeting Programmed Cell Death in Acquired Sensorineural Hearing Loss: Ferroptosis, Necroptosis, and Pyroptosis.Neuroscience bulletin · 2025Review
- Analysis and identification of mitochondria-related genes associated with age-related hearing loss.BMC genomics · 2025Article
- Bioinformatics approach reveals the critical role of inflammation-related genes in age-related hearing loss.Scientific reports · 2025Article
- Association between household solid fuel use and dual sensory impairment in a Chinese population: a retrospective cohort study.Frontiers in public health · 2025Article
- From genomic discovery to application in age-related hearing loss: a global bibliometric and cross-ethnic analysis.Frontiers in aging neuroscience · 2025Article
- Upregulation of the CaAging cell · 2024Article
- CORM‑2 reduces cisplatin accumulation in the mouse inner ear and protects against cisplatin-induced ototoxicity.Journal of advanced research · 2024Article
- Suppression of the TGF-β signaling exacerbates degeneration of auditory neurons in kanamycin-induced ototoxicity in mice.Scientific reports · 2024Article
- Development of Chinese herbal medicine for sensorineural hearing loss.Acta pharmaceutica Sinica. B · 2024Review
- Dialogue between mitochondria and endoplasmic reticulum-potential therapeutic targets for age-related cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Re-telling the story of aminoglycoside ototoxicity: tales from sub-Saharan Africa.Frontiers in neurology · 2024Article
- Sex differences in hearing impairment due to diet-induced obesity in CBA/Ca mice.Biology of sex differences · 2023Article
- Mitochondrial form and function in hair cells.Hearing research · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Age-related hearing loss (ARHL) is an irreversible, progressive neurodegenerative disorder and is presently untreatable. Previous studies using animal models have suggested mitochondrial damage and programmed cell death to be involved with ARHL. Thus, we further investigated the pathophysiologic role of mitochondria and necroptosis in aged C57BL/6J male mice. Aged mice (20 months old) exhibited a significant loss of hearing, number of hair cells, neuronal fibers, and synaptic ribbons compared to young mice. Ultrastructural analysis of aged cochleae revealed damaged mitochondria with absent or disorganized cristae. Aged mice also showed significant decrease in cochlear blood flow, and exhibited increase in gene expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3) and the pseudokinase mixed-lineage kinase domain-like (MLKL). Immunofluorescence (IF) assays of cytochrome C oxidase I (COX1) confirmed mitochondrial dysfunction in aged cochleae, which correlated with the degree of mitochondrial morphological damage. IF assays also revealed localization and increased expression of RIPK3 in sensorineural tissues that underwent significant necroptosis (inner and outer hair cells and stria vascularis). Together, our data shows that the aging cochlea exhibits damaged mitochondria, enhanced synthesis of proinflammatory cytokines, and provides new evidence of necroptosis in the aging cochlea in in vivo.
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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.