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SIRT1/PGC-1α/Mfn2通路调节VSMC中的线粒体平衡,以减轻与衰老相关的血管化

Chao Wu¹, Zufei Wu¹, Long Hu¹

¹Cardiology Department, Xuancheng People's Hospital, No. 15 Huancheng North Road, Xuancheng District, Xuancheng City, 242000, Anhui Province, China.

Scientific reports

|October 31, 2025

概括

沉默信息调节器1 (SIRT1) 激活通过恢复线粒体功能和促进血管光滑肌细胞 (VSMC) 中的SIRT1/PGC-1α/Mfn2通路来抑制与年龄相关的血管化. 这为动脉疾病提供了潜在的治疗点.

科学领域:

血管生物学血管生物学
线粒体生物学线粒体生物学
衰老研究研究衰老研究

背景情况:

与衰老相关的血管化是老年人中动脉疾病的重要因素.
线粒体融合/裂变不平衡与血管化有关,静音信息调节器1 (SIRT1) 显示有保护作用.
提升SIRT1的调节可以减轻血管光滑肌细胞 (VSMC) 中的线粒体损伤.

研究的目的:

研究SIRT1对血管化的抑制作用.
阐明涉及线粒体通路的潜在分子机制.

主要方法:

在VSMCs中建立的血管衰老模型,通过β-galactosidase染色证实.
使用转染,SIRT1的过度表达和PGC-1α的淘汰,通过RT-qPCR和Western Blot进行验证.
评估血管化,线粒体功能 (膜潜力,形态,ROS,ATP) 和关键通路蛋白 (SIRT1/PGC-1α/Mfn2).

主要成果:

衰老的VSMCs表现出增加的β-galactosidase和化,线粒体潜力和融合减少.
在衰老的VSMC中观察到SIRT1/PGC-1α/Mfn2通路的减少表达.
SIRT1的过度表达使衰老特征正常化,增强了PGC-1α和Mfn2的表达,减少了细胞亡和ROS,增加了ATP的分泌.
抑制PGC-1α减弱了SIRT1过度表达的有益作用.

结论:

SIRT1通过调节SIRT1/PGC-1α/Mfn2通路并改善线粒体功能来抑制与年龄相关的血管化.
这一途径代表了线粒体介导的血管衰老中的新机制.
SIRT1及其下游目标为预防和治疗老年人动脉疾病提供了潜在的治疗目标.

关键词:

衰老的衰老衰老的衰老线粒体的恒常性平衡.通过SIRT1/PGC-1α-ERRα/Mfn2进行信号传输.血管化是因为血管化.血管光滑肌细胞是血管光滑肌细胞

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