Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions

Abstract

Hearing loss profoundly affects social engagement, mental health, cognition, and brain development, with sensorineural hearing loss (SNHL) being a major concern. Linked to ototoxic medications, ageing, and noise exposure, SNHL presents significant treatment challenges, highlighting the need for effective prevention and regeneration strategies. Ferroptosis, a distinct form of cell death featuring iron-dependent lipid peroxidation, has garnered interest due to its potential role in cancer, ageing, and neuronal degeneration, especially hearing loss. The emerging role of ferroptosis as a crucial mediator in SNHL suggests that it may offer a novel therapeutic target for otoprotection. This review aims to summarise the intricate connection between ferroptosis and SNHL, offering a fresh perspective for exploring targeted therapeutic strategies that could potentially mitigate cochlear cells damage and enhance the quality of life for individuals with hearing impairments.

Keywords: Hearing loss; ferroptosis; otoprotection.

Figure 1.

The key molecular pathways of ferroptosis. (Drawn by Y.C., X.Li., Y.L., and Y.Y.).

Figure 2.

Key molecular pathways involved in ferroptosis and hearing loss. The key molecular pathways in hearing loss caused by cisplatin, aminoglycosides, sevoflurane administration, ageing, noise exposure, and otitis media were summarised. (Drawn by T.J., Z.C., and J.J.).