Wei, Y., Zhang, Y., Cao, W., Cheng, N., Xiao, Y., Zhu, Y., Xu, Y., Zhang, L., Guo, L., Song, J., Sha, S. H., Shao, B., Ma, F., Yang, J., Ying, Z., He, Z., Chai, R., Fang, Q., & Yang, J. (Accepted/In press). RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation. Advanced Science. https://doi.org/10.1002/advs.202407880
Wei, Yongjie ; Zhang, Yuhua ; Cao, Wei et al. / RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation. In: Advanced Science. 2025.
@article{f6496aac6b064eeb9ed204d4b3b87fb5,
title = "RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation",
abstract = "Age-related hearing loss is characterized by senescent inner ear hair cells (HCs) and reduced autophagy. Despite the improved understanding of these processes, detailed molecular mechanisms underlying cochlear HC senescence remain unclear. Transcription Factor EB (TFEB), a key regulator of genes associated with autophagy and lysosomes, crucially affects aging-related illnesses. However, intricate regulatory networks that influence TFEB activity remain to be thoroughly elucidated. The findings revealed that RONIN (THAP11), through its interaction with host cell factor C1 (HCF1/HCFC1), modulated the transcriptional activity of Tfeb, thus contributing to the mitigation (D-galatactose [D-gal]) senescent HC loss. Specifically, RONIN overexpression improved autophagy levels and lysosomal activity and attenuated changes associated with the senescence of HCs triggered by D-gal. These findings highlight the possibility of using RONIN as a viable therapeutic target to ameliorate presbycusis by enhancing the TFEB function.",
keywords = "aging-related hearing loss, autophagy, hair cell, RONIN/THAP11, Tfeb",
author = "Yongjie Wei and Yuhua Zhang and Wei Cao and Nan Cheng and Yun Xiao and Yongjun Zhu and Yan Xu and Lei Zhang and Lingna Guo and Jun Song and Sha, {Su hua} and Buwei Shao and Fang Ma and Jingwen Yang and Zheng Ying and Zuhong He and Renjie Chai and Qiaojun Fang and Jianming Yang",
note = "Publisher Copyright: {\textcopyright} 2025 The Author(s). Advanced Science published by Wiley-VCH GmbH.",
year = "2025",
doi = "10.1002/advs.202407880",
language = "English",
journal = "Advanced Science",
issn = "2198-3844",
publisher = "Wiley-VCH Verlag",
}
Wei, Y, Zhang, Y, Cao, W, Cheng, N, Xiao, Y, Zhu, Y, Xu, Y, Zhang, L, Guo, L, Song, J, Sha, SH, Shao, B, Ma, F, Yang, J, Ying, Z, He, Z, Chai, R, Fang, Q & Yang, J 2025, 'RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation', Advanced Science. https://doi.org/10.1002/advs.202407880
RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation. / Wei, Yongjie; Zhang, Yuhua; Cao, Wei et al.
In:
Advanced Science, 2025.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation
AU - Wei, Yongjie
AU - Zhang, Yuhua
AU - Cao, Wei
AU - Cheng, Nan
AU - Xiao, Yun
AU - Zhu, Yongjun
AU - Xu, Yan
AU - Zhang, Lei
AU - Guo, Lingna
AU - Song, Jun
AU - Sha, Su hua
AU - Shao, Buwei
AU - Ma, Fang
AU - Yang, Jingwen
AU - Ying, Zheng
AU - He, Zuhong
AU - Chai, Renjie
AU - Fang, Qiaojun
AU - Yang, Jianming
N1 - Publisher Copyright:
© 2025 The Author(s). Advanced Science published by Wiley-VCH GmbH.
PY - 2025
Y1 - 2025
N2 - Age-related hearing loss is characterized by senescent inner ear hair cells (HCs) and reduced autophagy. Despite the improved understanding of these processes, detailed molecular mechanisms underlying cochlear HC senescence remain unclear. Transcription Factor EB (TFEB), a key regulator of genes associated with autophagy and lysosomes, crucially affects aging-related illnesses. However, intricate regulatory networks that influence TFEB activity remain to be thoroughly elucidated. The findings revealed that RONIN (THAP11), through its interaction with host cell factor C1 (HCF1/HCFC1), modulated the transcriptional activity of Tfeb, thus contributing to the mitigation (D-galatactose [D-gal]) senescent HC loss. Specifically, RONIN overexpression improved autophagy levels and lysosomal activity and attenuated changes associated with the senescence of HCs triggered by D-gal. These findings highlight the possibility of using RONIN as a viable therapeutic target to ameliorate presbycusis by enhancing the TFEB function.
AB - Age-related hearing loss is characterized by senescent inner ear hair cells (HCs) and reduced autophagy. Despite the improved understanding of these processes, detailed molecular mechanisms underlying cochlear HC senescence remain unclear. Transcription Factor EB (TFEB), a key regulator of genes associated with autophagy and lysosomes, crucially affects aging-related illnesses. However, intricate regulatory networks that influence TFEB activity remain to be thoroughly elucidated. The findings revealed that RONIN (THAP11), through its interaction with host cell factor C1 (HCF1/HCFC1), modulated the transcriptional activity of Tfeb, thus contributing to the mitigation (D-galatactose [D-gal]) senescent HC loss. Specifically, RONIN overexpression improved autophagy levels and lysosomal activity and attenuated changes associated with the senescence of HCs triggered by D-gal. These findings highlight the possibility of using RONIN as a viable therapeutic target to ameliorate presbycusis by enhancing the TFEB function.
KW - aging-related hearing loss
KW - autophagy
KW - hair cell
KW - RONIN/THAP11
KW - Tfeb
UR - http://www.scopus.com/inward/record.url?scp=85218698570&partnerID=8YFLogxK
U2 - 10.1002/advs.202407880
DO - 10.1002/advs.202407880
M3 - Article
AN - SCOPUS:85218698570
SN - 2198-3844
JO - Advanced Science
JF - Advanced Science
ER -
Wei Y, Zhang Y, Cao W, Cheng N, Xiao Y, Zhu Y et al. RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation. Advanced Science. 2025. doi: 10.1002/advs.202407880