ArticleOxidative medicine and cellular longevity2022
Nrf2 Knockout Affected the Ferroptosis Signaling Pathway against Cisplatin-Induced Hair Cell-Like HEI-OC1 Cell Death.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- CarboxymethylatedFood science & nutrition · 2026Article
- Cycloastragenol Protects Against Cisplatin-Induced Cochlear Hair Cell Apoptosis via the PI3K/Akt/mTOR Pathway.Cellular and molecular neurobiology · 2026Article
- Navigating the Genetic Risk of Chemotherapy-Induced Hearing Loss in the Stria Vascularis.Clinical pharmacology and therapeutics · 2026Review
- Article
- Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Targeting Programmed Cell Death in Acquired Sensorineural Hearing Loss: Ferroptosis, Necroptosis, and Pyroptosis.Neuroscience bulletin · 2025Review
- Development of the inner ear and regeneration of hair cells after hearing impairment.Fundamental research · 2025Review
- Studies on the mechanism of ototoxic action of cisplatin and the antagonistic effect of polyphenolic compounds.Frontiers in pharmacology · 2025Review
- Article
- Hearing loss during chemotherapy: prevalence, mechanisms, and protection.American journal of cancer research · 2024Review
- Effects of Nutraceuticals on Cisplatin-Induced Cytotoxicity in HEI-OC1 Cells.International journal of molecular sciences · 2023Article
- Cisplatin ototoxicity mechanism and antagonistic intervention strategy: a scope review.Frontiers in cellular neuroscience · 2023Review
- The role of autophagy and ferroptosis in sensorineural hearing loss.Frontiers in neuroscience · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is a well-known and widely used anticancer drug with high therapeutic efficacy in solid tumors; however, side effects are common with its use. Because cisplatin can be retained in the cochlea, ototoxicity leading to hearing loss limits its clinical applications. Here, we report that Nrf2 knockout (KO) strongly increased cisplatin resistance in HEI-OC1 cells, which are immortalized cells from the murine organ of Corti. The underlying mechanism of this phenomenon was uncovered, and an important novel therapeutic target for combating cisplatin-induced hearing loss was identified. Preliminary investigations determined that Nrf2 KO markedly decreased TfR1 protein levels and increased GPX4 protein levels. Thus, ferroptosis may protect organisms from cisplatin-induced cell death. Furthermore, Nrf2 KO cells were resistant to the classical ferroptosis inducers RSL3 and erastin, providing solid evidence that Nrf2 KO inhibits ferroptosis and that knocking out Nrf2 may be a new clinical strategy to prevent cisplatin-induced hearing loss.
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