ArticleScience advances2024
In silico transcriptome screens identify epidermal growth factor receptor inhibitors as therapeutics for noise-induced hearing loss.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Pharmacologic Inhibition of JAK1/2 Potentiates Aminoglycoside-Induced Ototoxicity.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2026Article
- Supporting cells orchestrate noise-induced hearing loss via a Gasdermin D-dependent signaling loop with hair cells.Nature communications · 2025Article
- The influence of targeted therapies in the inner ear.Frontiers in pharmacology · 2025Review
- GPR83 protects cochlear hair cells against ibrutinib-induced hearing loss through AKT signaling pathways.Frontiers in medicine · 2025Article
- Paving the way for better ototoxicity assessments in cisplatin therapy using more reliable animal models.Frontiers in cellular neuroscience · 2025Article
- Occupational epidemiological characteristics of noise-induced hearing loss and the impact of combined exposure to noise and dust on workers' hearing-a retrospective study.Frontiers in public health · 2024Article
- Age-related hearing loss in older adults: etiology and rehabilitation strategies.Frontiers in neuroscience · 2024Review
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Abstract
Noise-induced hearing loss (NIHL) is a common sensorineural hearing impairment that lacks U.S. Food and Drug Administration-approved drugs. To fill the gap in effective screening models, we used an in silico transcriptome-based drug screening approach, identifying 22 biological pathways and 64 potential small molecule treatments for NIHL. Two of these, afatinib and zorifertinib [epidermal growth factor receptor (EGFR) inhibitors], showed efficacy in zebrafish and mouse models. Further tests with EGFR knockout mice and EGF-morpholino zebrafish confirmed their protective role against NIHL. Molecular studies in mice highlighted EGFR's crucial involvement in NIHL and the protective effect of zorifertinib. When given orally, zorifertinib was found in the perilymph with favorable pharmacokinetics. In addition, zorifertinib combined with AZD5438 (a cyclin-dependent kinase 2 inhibitor) synergistically prevented NIHL in zebrafish. Our results underscore the potential for in silico transcriptome-based drug screening in diseases lacking efficient models and suggest EGFR inhibitors as potential treatments for NIHL, meriting clinical trials.
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