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化物诱导心血管系统损伤的新机制通过调节p53/miR200c-3p在内皮功能障碍期间

Chao Zhang¹, Yue Wang², Fengya Huang²

¹Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, People's Republic of China; NHC Key Laboratory of Etiology and Epidemiology(Harbin Medical University), People's Republic of China; Joint Key Laboratory of Endemic Diseases, Harbin Medical University, Guizhou Medical University, Xi'an Jiaotong University, People's Republic of China.

Environmental research

|February 14, 2025

概括

化物暴露是高血压的危险因素,风险增加了56.5%. 化物还通过氧化应激和激活p53/miR-200c-3p通路引起内皮细胞功能障碍.

科学领域:

环境健康环境健康
心血管科学心血管科学
毒理学毒理学毒理学

背景情况:

化物对心血管系统的损害是一个公共卫生问题,对化物引起的心血管损伤的流行病学数据有限.
内皮细胞 (EC) 功能对于心血管疾病 (CVD) 诊断至关重要,但化物的破坏机制仍然不清楚.

研究的目的:

调查化物暴露与人口中高血压风险之间的关联.
探索化物诱导的EC功能损伤背后的机制.

主要方法:

流行病学研究将尿液中化物水平与高血压风险相关联.
在体内 (大鼠化模型) 和体内 (ECs) 使用化 (NaF) 的研究.
分析EC粘附,屏障功能,氧化应激标志物 (ROS,MDA,GPx4,SOD) 和信号通路 (p53/miR-200c-3p).

主要成果:

尿路化物度增加与高血压风险增加1.565倍有关.
NaF诱导了ECs的抗粘附性,屏障功能障碍,降低了eNOS/NO,并增加了ACE,vWF,ICAM-1,VCAM-1,ET-1.
NaF触发了氧化应激 (增加了ROS/MDA,减少了GPx4/SOD) 并通过ROS激活了p53/miR-200c-3p轴,导致内皮功能障碍.

结论:

化物暴露是高血压的重要危险因素.
化物通过氧化应激和p53/miR-200c-3p信号通路诱导EC功能障碍.
研究结果阐明了化物引起的心血管损伤的机制,为预防和治疗提供了理论基础.

关键词:

地方性化症地方性化症内皮质功能障碍内皮质功能障碍在高血压的高血压.p53/miR-200c-3ppp3p/miR-200c-3pp3p/miR-200c-3p3p/miR-200c-3p3p/miR-200c-3p3p/miR-200c-3p3p/miR-200c-3p3p/miR-200c-3p3p/miR-200c-3p

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