ArticleCell death & disease2011
Short interfering RNA against STAT1 attenuates cisplatin-induced ototoxicity in the rat by suppressing inflammation.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 141 citations in OpenAlex.
- Local application of otoprotective compounds other than sodium thiosulfate to prevent cisplatin-induced hearing loss: a systematic review.Drug delivery · 2026Pooled it
- The Chemoprotective Potentials of Alpha-lipoic Acid against Cisplatin-induced Ototoxicity: A Systematic Review.Current medicinal chemistry · 2024Pooled it
- Article
- From Ototoxicity to Otoprotection: Mechanism and Protective Strategies in Cisplatin Therapy.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Strategies to Mitigate Cisplatin-Induced Ototoxicity: A Literature Review of Protective Agents, Mechanisms, and Clinical Gaps.Audiology research · 2025Review
- Differential effect of targeting cisplatin-induced nitrative stress using MnTBAP in auditory and cancer cells.Current research in toxicology · 2025Article
- Studies on the mechanism of ototoxic action of cisplatin and the antagonistic effect of polyphenolic compounds.Frontiers in pharmacology · 2025Review
- Role of RGS17 in cisplatin-induced cochlear inflammation and ototoxicity via caspase-3 activation.Frontiers in immunology · 2025Article
- Enhancing biocompatibility of the brain-machine interface: A review.Bioactive materials · 2024Review
- Advances in the Study of Etiology and Molecular Mechanisms of Sensorineural Hearing Loss.Cell biochemistry and biophysics · 2024Review
- Macrophage depletion protects against cisplatin-induced ototoxicity and nephrotoxicity.Science advances · 2024Article
- Nuciferine Protects Cochlear Hair Cells from Ferroptosis through Inhibiting NCOA4-Mediated Ferritinophagy.Antioxidants (Basel, Switzerland) · 2024Article
- Potential of oligonucleotide- and protein/peptide-based therapeutics in the management of toxicant/stressor-induced diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Otoprotection against aminoglycoside- and cisplatin-induced ototoxicity focusing on the upstream drug uptake pathway.Journal of the Chinese Medical Association : JCMA · 2024Review
- Hearing loss during chemotherapy: prevalence, mechanisms, and protection.American journal of cancer research · 2024Review
- Apoptosis, autophagy, ferroptosis, and pyroptosis in cisplatin-induced ototoxicity and protective agents.Frontiers in pharmacology · 2024Review
- Recent Therapeutic Progress and Future Perspectives for the Treatment of Hearing Loss.Biomedicines · 2023Review
- Molecular Characteristics of Cisplatin-Induced Ototoxicity and Therapeutic Interventions.International journal of molecular sciences · 2023Review
- Macrophage Depletion Protects Against Cisplatin-Induced Ototoxicity and Nephrotoxicity.bioRxiv : the preprint server for biology · 2023Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cisplatin is widely used for treating various solid tumors. However, this drug produces dose-limiting ototoxicity and nephrotoxicity, which significantly reduce the quality of life of cancer patients. While nephrotoxicity could be alleviated by diuresis, there is currently no approved treatment for hearing loss. Previous studies show that the ROS and inflammation are major contributors to cisplatin-induced hearing loss. In this study, we show that ROS trigger the inflammatory process in the cochlea by activating signal transducer and activator of transcription-1 (STAT1). Activation of STAT1 activation was dependent on ROS generation through NOX3 NADPH oxidase, knockdown of which by siRNA reduced STAT1 activation. Moreover, STAT1 siRNA protected against activation of p53, reduced apoptosis, reduced damage to OHCs and preserved hearing in rats. STAT1 siRNA attenuated the increase in inflammatory mediators, such as TNF-α, inhibition of which protected cells from cisplatin-mediated apoptosis. Finally, we showed that trans-tympanic administration of etanercept, a TNF-α antagonist, protected against OHC damage and cisplatin-induced hearing loss. These studies suggest that controlling inflammation by inhibition of STAT1-dependent pathways in the cochlea could serve as an effective approach to treat cisplatin ototoxicity and improve the overall quality of life for cancer patients.
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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.