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RONIN/HCF1-TFEB Axis Protects Against D-Galactose-Induced Cochlear Hair Cell Senescence Through Autophagy Activation
Yongjie Wei1, Yuhua Zhang1, Wei Cao1
1Department of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|February 22, 2025
Summary
Researchers identified RONIN (THAP11) as a key factor in mitigating age-related hearing loss. By modulating Transcription Factor EB (TFEB) activity, RONIN enhances cellular repair mechanisms in aging cochlear hair cells.
Area of Science:
- Otolaryngology and Aging Research
- Cellular Senescence and Autophagy Mechanisms
- Molecular Biology of Hearing Loss
Background:
- Age-related hearing loss (presbycusis) involves senescent cochlear hair cells (HCs) and decreased autophagy.
- Molecular pathways driving cochlear HC senescence are not fully understood.
- Transcription Factor EB (TFEB) regulates autophagy and lysosomal function, impacting aging.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying cochlear HC senescence.
- To investigate the role of TFEB regulatory networks in aging inner ear cells.
- To identify potential therapeutic targets for presbycusis.
Main Methods:
- Investigated the interaction between RONIN (THAP11) and host cell factor C1 (HCF1/HCFC1).
- Assessed the modulation of Tfeb transcriptional activity by RONIN.
- Utilized D-galactose (D-gal) to induce HC senescence in experimental models.
Main Results:
- RONIN, via HCF1/HCFC1 interaction, regulates Tfeb transcriptional activity.
- Overexpression of RONIN enhanced autophagy and lysosomal activity in HCs.
- RONIN attenuated D-gal-induced senescence and hair cell loss.
Conclusions:
- RONIN plays a crucial role in mitigating cochlear hair cell senescence.
- Enhancing TFEB function through RONIN offers a potential therapeutic strategy for presbycusis.
- RONIN represents a promising therapeutic target for age-related hearing loss.
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