通过调节p66Shcc,SIRT1通过调节p66Shcc在与年龄相关的白内障期间防止镜片上皮细胞衰老
Huirui Liu1,2, Liyao Sun1, Yu Mi3
1Eye Hospital, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Aging cell
|June 26, 2025
概括
尼古丁胺胺单核酸 (NMN) 激活SIRT1,减少镜片上皮细胞 (LEC) 中的氧化应激和线粒体功能障碍. 这一过程抑制了衰老,延缓了与年龄相关的白内障 (ARC) 的进展,并提供了一个新的治疗策略.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 老年学是一门学科.
背景情况:
- 镜片上皮细胞 (LEC) 衰老是与年龄相关的白内障 (ARC) 发病的一个关键因素.
- LEC衰老与氧化应激,线粒体功能障碍和蛋白质聚合有关.
研究的目的:
- 阐明与年龄相关的白内障 (ARC) 中LEC衰老的致病性.
- 研究SIRT1和p66Shc在LEC衰老中的作用.
- 评估尼古丁胺胺单核酸 (NMN) 作为ARC的治疗剂的潜力.
主要方法:
- 量化SIRT1和p66Shc的蛋白质表达.
- 测量了反应性氧物种 (ROS) 和线粒体超氧化物水平.
- 评估的衰老标志物 (p21,p53,SA-β-银酸酶染色).
- 进行了针对性的代谢分析,并评估了线粒体形态/功能.
- 在ARC大鼠中使用组织学染色和电子显微镜评估透镜老化.
主要成果:
- 在人类白内障,UVB诱导的老鼠模型和UVB处理的LEC中观察到SIRT1的下调和p66Shc的上调.
- SIRT1激活缓解了UVB诱导的氧化应激和线粒体功能障碍,抑制了p66Shc的表达.
- NMN治疗激活了SIRT1,减轻了与衰老相关的蛋白质异常,并改善了线粒体结构和功能.
结论:
- NMN激活SIRT1,抑制线粒体功能障碍,氧化应激和LEC衰老,从而延迟镜头的不透明性.
- 这种机制为预防和治疗与年龄相关的白内障 (ARC) 提供了一个新的策略.
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