线粒体功能障碍加剧了通过氧化应激诱导的PM2.5的环境剂量通过氧化应激诱导的血管内皮细胞损伤:干预研究和细胞实验的发现
Cunzhong Jiang1, Liyan Yang1, Lin Miao1
1Department of Toxicology, School of Public Health, Anhui Medical University, Hefei 230032, China; Key Laboratory of Environmental Toxicology of Anhui Higher Education Institutes, Anhui Medical University, Hefei 230032, China.
Ecotoxicology and environmental safety
|January 30, 2026
概括
细颗粒物 (PM2.5) 暴露会通过引起氧化应激和线粒体功能障碍而损害血管. 这会损害内皮细胞,通过特定的生物途径增加心血管风险.
科学领域:
- 环境健康 环境健康
- 心血管研究研究心血管研究
- 细胞生物学 细胞生物学
背景情况:
- 颗粒物 (PM2.5) 是一种已知的心血管风险因素.
- 将PM2.5与内皮功能障碍,线粒体健康和能量代谢联系在一起的确切机制尚不清楚.
研究的目的:
- 研究PM2.5暴露导致内皮功能障碍和心血管风险的机制性途径.
- 阐明线粒体平衡,mtDNA完整性和细胞能量代谢在PM2.5诱导的血管功能障碍中的作用.
主要方法:
- 一个随机,双盲交叉试验,涉及受控的PM2.5暴露.
- 在人静脉内皮细胞 (HUVEC) 的体外实验.
- 因果调解建模,细胞对氧化应激和线粒体功能的测试,以及代谢分析.
主要成果:
- 暴露于PM2.5增加了血清EGF,VEGFA和D-二次体,同时降低了PDGF,PON1,GSH-Px和mtDNA拷贝数.
- PM2.5诱导的内皮损伤,高反应性氧物种 (ROS),抑制的eNOS表达,和受损的氧化 (NO) 生物可用性.
- 观察到线粒体功能障碍 (结构损伤,膜潜力降低) 和生物能效受损 (抑制糖解,抑制脂肪酸氧化,减少ATP).
- 氧化应激部分介导PM2.5诱导的内皮功能障碍 (40.30-71.80%).
结论:
- 暴露于PM2.5会通过一个轴,包括氧化应激,线粒体功能障碍和内皮功能障碍,提高心血管风险.
- 这些发现揭示了一个关键的机制性途径,解释了PM2.5.5对人口健康的影响.
- 针对这些途径可能为缓解PM2.5相关心血管疾病提供新的策略.
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