SLC26A4-gene mutations are a frequent cause of hereditary HearingLoss.
https://doi.org/10.1172/JCI193812 Here, Tsai et al. report that targeted AAV delivery to the endolymphatic sac and cochlear lateral wall restores auditory physiology and ameliorates cochlear pathology in a mouse model of Slc26a4-related deafness. Pendred syndrome DFNB4.
The image shows an AAV-GFP–transduced spiral prominence, a structure within the cochlear lateral wall. GFP (green) marks successfully transduced cells, phalloidin-568 (red) labels the actin cytoskeleton, and DAPI (blue) stains nuclei, highlighting efficient gene transfer to inner ear tissues essential for auditory function.
Address correspondence to: Chen-Chi Wu, Department of Otolaryngology, National Taiwan University Hospital, No. 1, Changde St., Zhongzheng Dist., Taipei City 100,229, Taiwan. Phone: 886.2.2312.3456; Email: [email protected]. Or to: Yen-Fu Cheng, Department of Medical Research, Taipei Veterans General Hospital, No. 201, Sec. 2, Shipai Rd., Beitou District, Taipei City 11,217, Taiwan. Phone: 886.2.2875.7642; Email: [email protected].
Find articles by Tsai, Y. in: | Google Scholar
1Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.








