ArticleFrontiers in immunology2025
Role of RGS17 in cisplatin-induced cochlear inflammation and ototoxicity via caspase-3 activation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Paeonol Alleviate Cisplatin- and Noise-Induced Hearing Loss by Preserving Hair Cell Ribosome Biogenesis.CNS neuroscience & therapeutics · 2026Article
- Review
- RGS14 promotes the progression of hepatocellular carcinoma by activating the cAMP/PKA/CREB signaling pathway.Journal of cancer research and clinical oncology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is a chemotherapy drug used to treat different solid tumors, including ovarian, bladder, lung, and head and neck cancers. One of its significant side effects is ototoxicity, especially when high doses are required. Cisplatin-induced ototoxicity is associated with increased cochlear cell death resulting from DNA damage, caspase activation, oxidative stress, inflammation, and glutamate excitotoxicity. The regulator of G protein signaling 17 (RGS17), a member of the RGS-RZ subfamily, hastens the hydrolysis of GTP to GDP on the G
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