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Cidea Targeting Protects Cochlear Hair Cells and Hearing Function From Drug- and Noise-Induced Damage
Shasha Zhang1, Ruiying Qiang2, Yuan Zhang3,4
1Southeast University Shenzhen Research Institute, Shenzhen, 518063, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|November 20, 2025
Summary
The apoptosis-inducing gene Cidea exacerbates hair cell loss in sensorineural hearing loss (SNHL). Inhibiting Cidea protects against noise- and drug-induced hearing damage, offering a potential SNHL therapeutic target.
Area of Science:
- Otolaryngology
- Molecular Biology
- Genetics
Background:
- Acquired sensorineural hearing loss (SNHL) results from hair cell (HC) damage, with limited clinical treatments.
- The apoptosis-inducing gene Cidea's role in SNHL is not well understood.
Purpose of the Study:
- Investigate the role of Cidea in SNHL.
- Explore Cidea as a therapeutic target for SNHL.
Main Methods:
- Examined Cidea expression in neomycin-damaged HCs.
- Utilized Cidea knockout (Cidea-/-) mice to assess HC apoptosis.
- Developed a CRISPR/SlugCas9-HF gene-editing therapy delivered via AAV to target Cidea.
Main Results:
- Cidea expression increased in neomycin-damaged HCs.
- Cidea deficiency protected HCs from neomycin and noise-induced apoptosis in vivo.
- CRISPR/SlugCas9-HF gene editing of Cidea reduced HC loss in SNHL models.
Conclusions:
- Cidea plays a significant role in HC apoptosis contributing to SNHL.
- Targeting Cidea presents a promising therapeutic strategy for preventing SNHL caused by ototoxic drugs and noise exposure.
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