Cisplatin-induced ototoxicity limits its clinical utility and may adversely impact cochlear implant outcomes. This study investigated the role of the HES1/PI3K/AKT/mTOR signaling axis in cisplatin-evoked cytotoxicity in HEI-OC1 auditory cells....
No actionable clinical change yet; this is preclinical mechanistic research, but the pathway identified could become a future drug target to protect hearing in patients receiving cisplatin chemotherapy.
Identifying the molecular mechanism behind cisplatin-induced hearing loss opens a potential therapeutic window to prevent ototoxicity (medication-related hearing damage) without compromising cancer treatment efficacy.
- 01Study identifies the HES1/PI3K/AKT/mTOR signaling pathway as mechanistically involved in cisplatin-induced hearing loss.
- 02Cisplatin is a widely used chemotherapy agent with well-documented ototoxic (hearing-damaging) side effects.
- 03Findings are preclinical — likely animal or in-vitro — limiting direct clinical translation at this stage.
- 04Authors suggest implications for cochlear implant outcomes in cisplatin-treated patients.
- 05The pathway may represent a novel drug target for otoprotective strategies in oncology patients.
The HES1/PI3K/AKT/mTOR signaling pathway plays a mechanistic role in cisplatin-induced sensorineural hearing loss.
studypartially supportedModulating this pathway may have implications for cochlear implant outcomes in patients treated with cisplatin.
opinionunclear- PMID
- 42350477
- DOI
- 10.1038/s41598-026-56936-1.
- Journal
- Scientific Reports
- Publication type
- research_article
- Evidence level
- 4
- Population
- Preclinical model (animal or in-vitro) of cisplatin-induced sensorineural hearing loss
- Intervention
- Mechanistic investigation of HES1/PI3K/AKT/mTOR signaling in cisplatin-exposed cochlear tissue
- Comparator
- Untreated or control cochlear tissue
Primary outcomes
Role of HES1/PI3K/AKT/mTOR pathway in cisplatin-induced cochlear damage; Potential therapeutic targets for otoprotection