罗宁/HCF1-TFEB轴通过自激活保护D-银河糖诱导的耳毛细胞衰老
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
概括
研究人员确定了RONIN (THAP11) 作为减轻与年龄相关的听力损失的关键因素. 通过调节转录因子EB (TFEB) 的活性,RONIN增强了老化耳毛细胞中的细胞修复机制.
科学领域:
- 耳鼻喉科和衰老研究研究
- 细胞衰老和自机制的机制
- 听力损失的分子生物学
背景情况:
- 与年龄相关的听力损失 (听力衰弱) 涉及衰老的耳毛细胞 (HCs) 和自的减少.
- 驱动耳HC衰老的分子途径尚未完全理解.
- 转录因子EB (TFEB) 调节自和溶酶体功能,影响衰老.
研究的目的:
- 阐明耳HC衰老背后的分子机制.
- 研究TFEB调节网络在老化内耳细胞中的作用.
- 为了确定可能的治疗对象的presbycusis.
主要方法:
- 研究了RONIN (THAP11) 和宿主细胞因子C1 (HCF1/HCFC1) 之间的相互作用.
- 评估了RONIN对Tfeb转录活性的调节.
- 在实验模型中利用D-银糖 (D-gal) 诱导HC衰老.
主要成果:
- 通过HCF1/HCFC1相互作用,RONIN调节Tfeb转录活动.
- 过度表达RONIN在HC中增强了自和溶酶体活性.
- 罗宁减弱的D-gal诱导的衰老和发细胞损失.
结论:
- 罗宁在缓解耳毛细胞衰老方面发挥着至关重要的作用.
- 通过RONIN增强TFEB功能提供了一个潜在的治疗策略.
- 罗宁代表了与年龄相关的听力损失的有前途的治疗标.
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