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在HUVEC中通过SIRT1/PGC-1α/SIRT3通路诱导的PM_2.5过早衰老

Qing Yan¹, Rao Zheng¹, Yi Li¹

¹Department of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou 215123, Jiangsu, China.

The Science of the total environment

|February 25, 2024

概括

细颗粒物 (PM2.5) 通过破坏SIRT1/PGC-1α/SIRT3通路,触发血管内皮细胞衰老,损害抗氧化防御,增加活性氧物种 (ROS). 这导致细胞循环停止和过早衰老.

科学领域:

心血管生物学心血管生物学
环境健康环境健康
细胞衰老细胞衰老

背景情况:

血管内皮细胞衰老是动脉样硬化发展的关键因素.
已知环境细颗粒物 (PM2.5) 在内皮细胞中诱导压力诱导的过早衰老 (SIPS).
将PM2.5暴露与内皮细胞衰老的确切机制需要进一步研究.

研究的目的:

研究PM2.5对血管内皮细胞衰老的影响.
阐明潜在的分子机制,重点关注SIRT1/PGC-1α/SIRT3通路和活性氧物种 (ROS).

主要方法:

人类静脉内皮细胞 (HUVECs) 暴露于PM2.5.5.
对衰老标志物 (SA-β-gal,P53/P21,P16) 和细胞周期进展的评估.
对SIRT1/PGC-1α/SIRT3信号通路和线粒体ROS水平的分析.
与ROS清除器 (MitoQ) 和SIRT1激活器 (SRT1720) 的干预.

主要成果:

暴露于PM2.5增加了HUVEC中的SA-β-gal活性,P53/P21和P16表达,导致G0/G1细胞周期停止.
PM2.5破坏了SIRT1/PGC-1α/SIRT3通路和细胞抗氧化剂防御系统.
清除线粒体ROS或激活SIRT1减弱的PM2.5诱导衰老标志物.

结论:

暴露于PM2.5会降低HUVEC中SIRT1/PGC-1α/SIRT3通路的调节,从而损害抗氧化防御.
这种损伤导致ROS积累,细胞循环抑制和压力诱导的过早衰老.
准这种途径可能提供针对PM2.5诱导的血管损伤的治疗策略.

关键词:

抗氧化剂防御的抗氧化剂防御在HUVECs中,在PM中{2.5)通过SIRT1/PGC-1α/SIRT3路径.压力引起的过早衰老.

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