ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Necroptosis and Apoptosis Contribute to Cisplatin and Aminoglycoside Ototoxicity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Hearing Impairment in South Africa and the Lessons Learned for Planetary Health Genomics: A Systematic Review.Omics : a journal of integrative biology · 2022Pooled it
- MLL1 downregulation drives hair cell ferroptosis via mitochondrial and endoplasmic reticulum stress mechanisms through PERK-eIF2α-ATF4-Chop and PI3K/Akt-Lrp1 signaling pathway.Chinese medical journal · 2026Article
- Quantifying the Silent Selection Pressure: Antimicrobial Stewardship and Gut Microbiome Integrity in the NICU and PICU.Biomedicines · 2026Article
- Mechanisms, prevention, and management of aminoglycoside-induced hearing loss in neonates and children: a translational review.Frontiers in pharmacology · 2026Review
- Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Vernonia amygdalina displays otoprotective effects via antioxidant pathway on cisplatin-induced hair cell loss in zebrafish.Archives of toxicology · 2025Article
- Effects of Methionine and Glutathione on Acute Ototoxicity Induced by Amikacin and Furosemide in an Animal Model of Hearing Threshold Decrease.Biomedicines · 2025Article
- Targeting Programmed Cell Death in Acquired Sensorineural Hearing Loss: Ferroptosis, Necroptosis, and Pyroptosis.Neuroscience bulletin · 2025Review
- Strategies to Mitigate Cisplatin-Induced Ototoxicity: A Literature Review of Protective Agents, Mechanisms, and Clinical Gaps.Audiology research · 2025Review
- Sarsasapogenin protects hair cells from cisplatin-induced ototoxicity by attenuating apoptosis and ferroptosis via alleviating oxidative stress.Frontiers in pharmacology · 2025Article
- Enhancing biocompatibility of the brain-machine interface: A review.Bioactive materials · 2024Review
- Notoginsenoside R1 Attenuates Cisplatin-Induced Ototoxicity by Inducing Heme Oxygenase-1 Expression and Suppressing Oxidative Stress.International journal of molecular sciences · 2024Article
- CORM‑2 reduces cisplatin accumulation in the mouse inner ear and protects against cisplatin-induced ototoxicity.Journal of advanced research · 2024Article
- Multiple mechanisms of aminoglycoside ototoxicity are distinguished by subcellular localization of action.bioRxiv : the preprint server for biology · 2024Article
- Nobiletin alleviates cisplatin-induced ototoxicity via activating autophagy and inhibiting NRF2/GPX4-mediated ferroptosis.Scientific reports · 2024Article
- Hearing loss during chemotherapy: prevalence, mechanisms, and protection.American journal of cancer research · 2024Review
- Multiple mechanisms of aminoglycoside ototoxicity are distinguished by subcellular localization of action.Frontiers in neurology · 2024Article
- The chiisanoside derivatives present in the leaves ofFrontiers in pharmacology · 2024Article
- Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury.Toxicological research · 2024Article
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Authors and funding
11 authors.
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Abstract
Ototoxic side effects of cisplatin and aminoglycosides have been extensively studied, but no therapy is available to date. Sensory hair cells, upon exposure to cisplatin or aminoglycosides, undergo apoptotic and necrotic cell death. Blocking these cell death pathways has therapeutic potential in theory, but incomplete protection and lack of therapeutic targets in the case of necrosis, has hampered the development of clinically applicable drugs. Over the past decade, a novel form of necrosis, termed necroptosis, was established as an alternative cell death pathway. Necroptosis is distinguished from passive necrotic cell death, in that it follows a cellular program, involving the receptor-interacting protein kinase (RIPK) 1 and RIPK3. In this study, we used pharmacological and genetic interventions in the mouse to test the relative contributions of necroptosis and caspase-8-mediated apoptosis toward cisplatin and aminoglycoside ototoxicity. We find that
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