Recently, the professor Xiaoting Jin’s group from department of labor Health and environmental health has great achievement on the effect of fine particulate matter (PM2.5) exposure on myocardial energy metabolism and its related mechanism. Relevant results have been published in Science of the Total Environment (TOP 1, Impact Factor：5.92）and Environmental Pollution (TOP 2, Impact Factor: 5.714) under the title of “Cardiac dysfunction and metabolic remodeling due to seasonally ambient fine particles exposure” and “Critical biomarkers for myocardial damage by fine particulate matter: Focused on PPARα-regulated energy metabolism”, respectively.
These studies mainly focused on seasonal PM2.5-induced cardiac dysfunction and metabolic remodeling, and the toxicity differences of PM2.5 samples from different sampling seasons and different exposure dosages were discussed. The results showed that seasonal haze caused cardiac dysfunctions and myocardial damage. Comparatively, winter PM2.5 exposure caused more severe cardiac toxicity than did summer haze samples, possibly due to the existence of different components and pollutant levels in seasonal hazes. To further investigate the possible mechanism, Jin’s team conducted research on pollution exposure for the selection and utilization of myocardial energy substrates, changes in key energy metabolism pathways and the effects of energy utilization and storage. Of note, low dose PM2.5 exposure induced the elevation of β-oxidation and TCA cycle as the compensation for the disturbed energy metabolism in animals, whereas high dose of PM2.5 exposure attenuated this process and the glycolysis levels were strikingly promoted, thus causing the reduced energy production and cardiac dysfunction. Meanwhile, the PPARα was found to be a pivotal role in the regulation of myocardial metabolic remodeling incurred by PM2.5. The findings on seasonal PM2.5 induced cardiac dysfunction and myocardial metabolic remodeling provided new insights into cardiovascular disease risks from haze exposure.
The professor Xiaoting Jin is the corresponding author of the two papers, and postgraduate students Jingxu Zhang and Ze Zhang are the first authors of the two articles, respectively. Cooperative units in this research included the Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, University of Shanxi and University of Karachi.
This work was financially supported by the National Natural cience Foundation of China (No. 219761 14, 21707085) and the Taishan Scholars Program of Shandong Province (NO. tsqn201909101).
Figure: Fine particulate matter exposure and energy metabolism remodeling of cardiomyocytes. (DOI: 10.1016/j.scitotenv.2020.137792)
Thesis links:
1. https://www.sciencedirect.com/science/article/pii/S0048969720313048?via%3Dihub
2. https://www.sciencedirect.com/science/article/pii/S0269749120310502?via%3Dihub
晋小婷教授团队在大气细颗粒物暴露与心肌能量代谢研究中取得重要成果
近日，我院劳动卫生与环境卫生系晋小婷教授团队在研究大气细颗粒物 (PM2.5) 暴露与心肌能量代谢方面取得重要成果，相关成果以“Cardiac dysfunction and metabolic remodeling due to seasonally ambient fine particles exposure”和“Critical biomarkers for myocardial damage by fine particulate matter: Focused on PPARα-regulated energy metabolism”为题分别发表于国际学术期刊《Science of the Total Environment》(TOP一区，影响因子：5.92）和《Environmental Pollution》(TOP二区，影响因子：5.714)。
本研究发现SD大鼠暴露于冬季或夏季PM2.5后，引起心肌结构和功能紊乱，诱发大鼠心力衰竭，且同等剂量冬季PM2.5影响大于夏季。进一步围绕心肌能量底物选择及利用、关键能量代谢途径变化、能量利用及储存，发现低剂量PM2.5暴露诱导细胞能量代谢代偿效应发生；而雾霾剂量PM2.5暴露引起心肌能量代谢重构，主要表现为脂肪酸代谢水平下降、糖降解水平升高；同时发现PPARα在颗粒物引起的心肌能量代谢重构中发挥关键调控作用。该系列工作首次围绕心肌能量代谢重构，解析雾霾剂量PM2.5诱导心力衰竭的可能分子机制，进而为大气颗粒物暴露引起的心血管疾病风险提出新见解，为城市雾霾防控的必要性提供科学依据。
晋小婷教授为两篇文章的通讯作者，硕士研究生张京旭和张泽分别为两篇文章的第一作者。本研究合作单位包括中国科学院生态环境研究中心，山西大学以及University of Karachi。
该课题得到国家自然科学基金（Nos. 21976114, 21707085, 21976114和91643203）和山东省泰山青年学者基金（tsqn201909101）的支持。
图：大气细颗粒物暴露与心肌细胞能量代谢重构（图片来自DOI: 10.1016/j.scitotenv.2020.137792）
论文链接：
1. https://www.sciencedirect.com/science/article/pii/S0048969720313048?via%3Dihub
2.https://www.sciencedirect.com/science/article/pii/S0269749120310502?via%3Dihub
