Cidea Targeting Protects Cochlear Hair Cells and Hearing Function From Drug‐ and Noise‐Induced Damage

Acquired sensorineural hearing loss (SNHL) is primarily caused by the damage or loss of hair cells (HCs), induced by factors such as noise exposure and ototoxic drugs. However, clinical treatments for SNHL remain limited. Here, the role of the apoptosis-inducing gene Cidea in SNHL is investigated. It is initially observed that Cidea expression is specifically increased in neomycin-damaged HCs at both the protein and mRNA levels. To further explore its role, Cidea knockout (Cidea-/-) mice are obtained, and it is found that the absence of Cidea effectively alleviates HC apoptosis caused by neomycin treatment and noise exposure in vivo. Moreover, a novel therapeutic strategy for SNHL has been developed by delivering CRISPR/SlugCas9-HF via AAV to edit Cidea, and this approach significantly reduced HC loss induced by both neomycin and noise exposure. These findings suggest that Cidea may serve as a promising target for the prevention of neomycin- and noise-induced SNHL in clinical settings.

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Publication Details

Journal
Advanced Science
Published
2025-11-20
DOI
https://doi.org/10.1002/advs.202517206
Citations
1
Primary Topic
Hearing, Cochlea, Tinnitus, Genetics
Type
article
Field-Weighted Citation Impact
1.46

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article

Cidea Targeting Protects Cochlear Hair Cells and Hearing Function From Drug‐ and Noise‐Induced Damage

Ruiying Qiang, Ying Ma, Tong Wei, Renjie Chai et al.
1 citations
Advanced Science
Hearing, Cochlea, Tinnitus, Genetics
1.46
article

Cidea Targeting Protects Cochlear Hair Cells and Hearing Function From Drug‐ and Noise‐Induced Damage

Ruiying Qiang, Ying Ma, Tong Wei, Renjie Chai, Jun Wan, Hairong Xiao, Yanqin Lin, Yuan Zhang, Tao Chen, Peng Li, Yongming Wang, Ying Dong, Xujun Tang, L. Xu, Shasha Zhang
article en
1 citations

Abstract

Acquired sensorineural hearing loss (SNHL) is primarily caused by the damage or loss of hair cells (HCs), induced by factors such as noise exposure and ototoxic drugs. However, clinical treatments for SNHL remain limited. Here, the role of the apoptosis-inducing gene Cidea in SNHL is investigated. It is initially observed that Cidea expression is specifically increased in neomycin-damaged HCs at both the protein and mRNA levels. To further explore its role, Cidea knockout (Cidea-/-) mice are obtained, and it is found that the absence of Cidea effectively alleviates HC apoptosis caused by neomycin treatment and noise exposure in vivo. Moreover, a novel therapeutic strategy for SNHL has been developed by delivering CRISPR/SlugCas9-HF via AAV to edit Cidea, and this approach significantly reduced HC loss induced by both neomycin and noise exposure. These findings suggest that Cidea may serve as a promising target for the prevention of neomycin- and noise-induced SNHL in clinical settings.

Advanced ScienceVol. 13(7)
University of Electronic Science and Technology of China (CN), Nantong University (CN), Prevention Institute (US), King Center (US), Zhengzhou University (CN), Zhongda Hospital Southeast University (CN), Nanjing Drum Tower Hospital (CN), Nanjing Hydraulic Research Institute (CN), Pudong Medical Center (CN), Center for Life Sciences (CN), Nanjing Institute of Environmental Sciences (CN), State Key Laboratory of Digital Medical Engineering (CN), Southeast University (CN), Tsinghua University (CN)
National Natural Science Foundation of China, Government of Jiangsu Province, Natural Science Foundation of Jiangsu Province, Basic and Applied Basic Research Foundation of Guangdong Province
Openalex Percentile: Top 15%
Hearing, Cochlea, Tinnitus, Genetics
1.46
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