大量流行病学调查研究表明PM2.5颗粒物对心血管系统有着复杂而重要的影响，是大气污染引发心血管疾病的重要启动因子。心脏的自律性是心脏最根本的生理功能，心脏自律性的异常会加剧或引发多种心血管疾病。然而，PM2.5颗粒物对心脏自律性这一重要生理功能的影响仍有待评估。因此，本课题采集广州、太原两地的PM2.5颗粒物，借助由KM小鼠和胚胎干细胞诱导的类窦房结细胞搭建的心脏自律性内外控制系统分析平台，阐明在急性应激和长期应激中，不同来源和组成成分的PM2.5颗粒物和心脏自律性内外控制系统的暴露-效应关系。在此基础上，从氧化应激、炎症反应、基因损伤、病理特征及电生理特性等相关层面着手，全面探究PM2.5颗粒物影响心脏自律性的机制。本课题将为全面评价PM2.5颗粒物的心脏内外自律系统风险提供清晰、准确的科学信息，并为PM2.5颗粒物相关疾病的预防和治疗靶点选择奠定理论基础。

A large number of epidemiological surveys show that the adverse effect of PM2.5 on cardiovascular system is complex and severe and PM2.5 is an important promoter for the cardiovascular diseases induced by atmospheric pollution. The automaticity of heart is a fundamental physiological function in our heart and its dysfunction will aggravate or induce various cardiovascular diseases. However, the effects of PM2.5 on automaticity of heart are still unclear. Here, we try to collect the PM2.5 sample from Guangzhou and Taiyuan to investigate the relationship between PM2.5 (different components, different sources) and the automaticity of heart (extracardiac system, intrinsic system) from an acute and long-term exposure by building up a research platform with KM mouse and embryonic stem cells derived sinoatrial node cells. On that basis, we will explore the detailed mechanisms of how PM2.5 affects the automaticity of heart from oxidative stress, inflammatory response, DNA damage, pathological features and electrophysiological properties. Our project will not only accurately estimate the risk of PM2.5 on cardiovascular system but also offer a scientific basis for future prevent and therapy of PM2.5 related diseases.