不同区域PM2.5浓度的增加均可导致易感人群心血管疾病（CVD）的发病率与病死率上升，但各地上升值差异较大，PM2.5中的组分不同可能是造成此差异的主要原因之一。但目前PM2.5中具体组分与CVD关系的研究主要在流行病学方面，只能提示某些组分与CVD的相关性，缺乏实验证据。为此，本项目拟开展以下工作：1）采用老年小鼠研究不同城市PM2.5暴露对个体血压、心脏功能、病理、心肌肥大及纤维化标志物的影响；2)通过不同城市PM2.5成分与心脏功能及心肌肥大/纤维化标志物的相关性分析，确定关键毒性组分；并在体内验证关键毒性组分诱导心脏功能紊乱及心肌肥大/纤维化的作用；3）体外培养心肌纤维细胞，结合多种抑制剂及RNA干扰技术解析PM2.5及其关键毒性组分引发心肌肥大/纤维化的分子机制及信号途径。旨在确定诱导CVD易感性增加的PM2.5关键毒性组分，为不同地区PM2.5健康防治提供科学依据和技术支持。

Elevation of particulate matter (PM)<2.5 in diameter (PM2.5) can accelerate cardiovascular disease–related mortality and morbidity to various degrees in different districts, especially in sensitive people. The different components of PM2.5 in various districts might be one of the important causes of cardiovascular disease hospital visits and mortality differences. However, existing researches about the association between the specific components of PM2.5 and cardiovascular disease focused mainly on epidemiological studies. It is absent of the experimental evidence. In the present study, 1）The effects of PM2.5 from different cities on blood pressure, cardiac function, cardiomyocyte hypertrophy and fibrosis will be studied on elderly mice. 2) The correlation analysis will be performed between the specific components of PM2.5 and markers of cardiac function, cardiomyocyte hypertrophy and fibrosis to find the key toxic components of triggering cardiovascular disease. We will confirm the key toxic components that induce cardiomyocyte hypertrophy and fibrosis in vivo. 3）The molecular mechanism and signal pathway of PM2.5 and its key toxic components triggering cardiomyocyte hypertrophy and fibrosis will be probed using cardiac fibroblasts in vitro. The work is undertaken to determine the key toxic components, which increase the CVD susceptibility, and provide scientific basis and technical support for preserving and treatment of human exposed to PM2.5 in different districts.