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准LARP1以缓解透镜上皮细胞的衰老:对线粒体功能障碍的机制性见解

Hang Qi¹, Liankun Sun², Jiannan Chai³

¹First Hospital of Jilin University, Changchun, 130021, China; Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.

Experimental eye research

|August 16, 2025

概括

与LA相关的蛋白1 (LARP1) 的上调驱动了透镜上皮细胞 (LEC) 通过损害线粒体功能而衰老. 抑制LARP1和压力颗粒的形成可能会延迟LEC衰老并预防白内障.

科学领域:

细胞生物学细胞生物学
眼科医生眼科眼科
衰老研究研究衰老研究

背景情况:

透镜上皮细胞 (LEC) 对透镜透明度至关重要,它们的老化有助于白内障的形成.
线粒体代谢是延缓LEC衰老的关键目标.
与LA相关的蛋白1 (LARP1) 影响线粒体功能,但其在LEC衰老中的作用尚不清楚.

研究的目的:

研究LARP1影响LEC衰老和线粒体功能的机制.
探索LARP1作为延迟LEC衰老的潜在治疗标.

主要方法:

使用D-银糖诱导LEC衰老.
使用siRNA.RNA进行LARP1敲击.
对线粒体氧化酸化 (OXPHOS) 功能的评估.
对NDUFB8和SDHBmRNA和蛋白质表达的分析.
研究应力颗粒 (SG) 的形成和抑制.

主要成果:

在D-银糖诱导的老化的LEC中,LARP1的调节显著上升.
通过LARP1 knockdown减弱了LEC衰老,并恢复了OXPHOS功能.
通过与它们的mRNA结合并形成SGs,LARP1抑制了NDUFB8和SDHB的表达,从而损害了OXPHOS.
SG抑制剂恢复了NDUFB8/SDHB的翻译,并减少了衰老标志物.

结论:

LARP1在LEC衰老中发挥着关键作用,通过通过SG介导的转化抑制损害线粒体OXPHOS功能.
针对LARP1和SG形成提供了潜在的策略来打击LEC衰老和延迟白内障的发展.

关键词:

衰老的衰老衰老的衰老在LARP1中使用LARP1.氧化酸化是一种氧化酸化.压力颗粒是一种压力颗粒.翻译翻译翻译翻译

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