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Systematic review identifies ferroptosis as a key mechanism in acquired sensorineural hearing loss

Systematic review identifies ferroptosis as a key mechanism in acquired sensorineural hearing loss
Photo by Etactics Inc / Unsplash
Key Takeaway
Note that ferroptosis-targeted interventions for sensorineural hearing loss are currently limited to preclinical research.

This systematic review explores the molecular pathways of ferroptosis and the progress of ferroptosis-targeted interventions in the context of sensorineural hearing loss. The scope includes drug-induced, noise-induced, and age-related hearing loss. The authors identify ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, as a key mechanism in acquired sensorineural hearing loss.

The review synthesizes advancements in interventions designed to target this cell death pathway. While the potential for otoprotective therapies is noted, the authors emphasize that the discussed interventions are currently limited to preclinical models. The transition from laboratory findings to clinical application is not yet established.

Significant gaps remain in the current literature, as the authors note that targeting ferroptosis is still largely preclinical. Future clinical translation will likely require the integration of novel technologies, such as single-cell omics and nano-delivery systems. Clinicians should interpret these findings as early-stage mechanistic insights rather than established therapeutic options.

Study Details

Study typeSystematic review
EvidenceLevel 1
PublishedMay 2026
View Original Abstract ↓
Sensorineural hearing loss (SNHL) is a major cause of disability worldwide, characterized by irreversible damage to cochlear hair cells and spiral ganglion neurons. Current treatments such as hearing aids and cochlear implants do not restore biological function. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a key mechanism in acquired SNHL, including drug-, noise-, and age-related forms. This review systematically outlines the core molecular pathways of ferroptosis in SNHL, summarizes recent advances in ferroptosis-targeted interventions, and critically discusses current challenges and translational prospects. Although still largely preclinical, targeting ferroptosis represents a promising strategy for developing otoprotective therapies. Future research integrating novel technologies such as nano-delivery systems and single-cell omics may accelerate clinical translation.
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