Plenty of epidemiological evidences have shown that ambient particulate matter (PM2.5) exposure increased the prevalence of cardiovascular disease, but the potential mechanism has not been known clearly. We established mice models by ambient PM2.5 exposure system to explore the adverse effects of PM2.5 on cardiac function in mice. Forty-eight C57BL/6 mice were randomly divided into 3 groups and exposed to filtered air (FA), unfiltered air (UA) and concentrated PM2.5 air (CA) for 8 or 16 weeks, 6 hours per day, 7 days per week, respectively. The changes of cardiac structure and function, histological analysis and related mechanism were investigated. The main manifestations of cardiac structure were cardiac hypertrophy and fibrosis in a dose- and time-dependent manner after PM2.5 exposure, which led to the decrease of cardiac systolic function. Cardiac hypertrophy in mice might be regulated by PI3K/Akt/FoxO1 signal. Cardiac fibrosis might be attributed to inflammatory infiltration caused by macrophage activation. Consequently, our data indicated that cardiac hypertrophy and fibrosis might be important factors of PM2.5-induced cardiac dysfunction in mice.

中文翻译：

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PM2.5引起的心脏功能障碍是通过FoxO1靶向的心肌肥大和巨噬细胞激活的纤维化引起的。

大量的流行病学证据表明，接触环境颗粒物（PM2.5）会增加心血管疾病的患病率，但其潜在机制尚不清楚。我们通过环境PM2.5暴露系统建立了小鼠模型，以探讨PM2.5对小鼠心脏功能的不利影响。48只C57BL / 6小鼠随机分为3组，分别暴露于过滤空气（FA），未过滤空气（UA）和浓PM2.5空气（CA）中，每天8天或16周，每天6小时，每天7天。一周。研究了心脏结构和功能的变化，组织学分析及相关机制。暴露于PM2.5后，心脏结构的主要表现为心脏肥大和纤维化，呈剂量和时间依赖性，这导致心脏收缩功能下降。小鼠心脏肥大可能受PI3K / Akt / FoxO1信号调节。心脏纤维化可能归因于巨噬细胞激活引起的炎症浸润。因此，我们的数据表明心脏肥大和纤维化可能是PM2.5诱导的小鼠心脏功能障碍的重要因素。