Drug-induced ototoxicity remains a clinically relevant challenge associated with the use of several essential pharmacological agents, because effective strategies to prevent permanent auditory or vestibular damage are still limited. Ototoxic drugs differ in their chemical structure, therapeutic indication, and mechanism of action, but their damaging effects converge on partially overlapping molecular events within...
✦ The floor
Discussion
Signed responses from readers of the wire.
No actionable change at this time — this is a foundational science review identifying protein targets; clinical translation awaits future drug or protective agent development.
Systematically cataloguing ototoxicity-related proteins lays the molecular groundwork needed to develop targeted drugs that could prevent or treat medication-induced hearing loss.
- 01Review maps proteins across four stages: drug entry, damage amplification, cell death, and endogenous protection.
- 02Structure-guided approach identifies specific molecular targets for potential otoprotective interventions.
- 03Covers multiple drug classes known to cause hearing damage (e.g., aminoglycosides, cisplatin).
- 04Endogenous otoprotective pathways are highlighted as potential therapeutic leverage points.
- 05Findings are preclinical/mechanistic — no direct patient management implications yet.
Specific proteins mediate drug entry into inner ear hair cells and contribute to ototoxic damage.
studypartially supportedEndogenous otoprotective responses can be mapped at the protein structure level and may represent therapeutic targets.
studypartially supported- PMID
- 42800300
- DOI
- 10.1016/j.heares.2026.109811.
- Journal
- Hearing Research
- Publication type
- review
- Evidence level
- 5
- Population
- Not applicable — protein/molecular structure review (no human or animal subjects)
- Intervention
- Structure-guided mapping of ototoxicity-related proteins
Primary outcomes
Identification of proteins involved in drug entry into inner ear cells; Characterisation of damage amplification and cell death execution mechanisms; Mapping of endogenous otoprotective protein responses