Targeting ferroptosis in sensorineural hearing loss: mechanisms, therapeutics, and translational prospects

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.