关于PM2.5暴露和心脏发育毒性之间的不良结果途径链接的概述
Chen Liang1,2, Ruiyang Ding1,2, Qinglin Sun1,2
1Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, China.
Environment & health (Washington, D.C.)
|October 30, 2024
概括
在发育过程中接触细颗粒物 (PM2.5) 会增加先天性心脏缺陷 (CHD) 的风险. 本综述概述了从PM2.5暴露到通过氧化应激和破坏细胞信号传递的心脏异常的途径.
科学领域:
- 环境健康 环境健康
- 发育毒理学 发展毒理学
- 心血管研究研究心血管研究
背景情况:
- 细颗粒物 (PM2.5) 是已知的出生缺陷的风险因素.
- 发育中的心脏特别容易受到环境毒素的影响.
- 现有的PM2.5心脏毒性研究缺乏机械整合.
研究的目的:
- 提出一个不良结果路径 (AOP) 框架,将PM2.5暴露与先天性心脏缺陷 (CHD) 联系起来.
- 阐明PM2.5引起的心脏发育毒性背后的分子机制.
主要方法:
- 对PM2.5和心脏发育的现有研究进行审查和整合.
- 适用不良结果路径 (AOP) 框架.
- 识别分子启动事件 (MIE) 和关键事件 (KE).
主要成果:
- 暴露于PM2.5会通过基碳化合物受体 (AhR) 激活和活性氧物种 (ROS) 产生毒性.
- ROS诱导导致氧化应激,DNA损伤,炎症和亡.
- 激活AhR抑制了Wnt/β-catenin信号传递,抑制了心肌细胞的分化.
- 心肌细胞分化和亡的损伤导致心脏结构和功能异常.
结论:
- 通过一系列关键事件,AOP框架成功地将PM2.5暴露与CHD联系起来.
- 了解这些机制对于评估PM2.5安全性和预防CHD至关重要.
- 本综述提供了PM2.5对心脏发育毒性的统一观点.
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