Citation: Xuyang Chai, Hiu-Lok Ngan, Yuanyuan Song, Zenghua Qi, Lifang Zhao, Wenqi Chen, Shanshan Chen, Zhenhua Yang, Ruijin Li, Chuan Dong, Zhu Yang, Zongwei Cai. Real-world PM_2.5 exposure induces prostaglandin disruption and low-density lipoprotein oxidation, exacerbating atherogenesis in ApoE^−/− mice[J]. Chinese Chemical Letters, ;2025, 36(9): 110671. doi: 10.1016/j.cclet.2024.110671 shu

Real-world PM_2.5 exposure induces prostaglandin disruption and low-density lipoprotein oxidation, exacerbating atherogenesis in ApoE^−/− mice

Xuyang Chai ^{a, 1} ,
Hiu-Lok Ngan ^{a, 1} ,
Yuanyuan Song ^a ,
Zenghua Qi ^b ,
Lifang Zhao ^c ,
Wenqi Chen ^c ,
Shanshan Chen ^c ,
Zhenhua Yang ^c ,
Ruijin Li ^c ,
Chuan Dong ^c ,
Zhu Yang ^{a, d, *,} ,
Zongwei Cai ^{a, b, *,}

a.
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China
b.
School of Environmental Science and Engineering, Guangdong University of Technology, Guangzhou 510006, China
c.
Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan 030006, China
d.
Department of Biology, Hong Kong Baptist University, Hong Kong, China

zyang@hkbu.edu.hk

zwcai@hkbu.edu.hk

Received Date: 9 July 2024
Revised Date: 18 October 2024
Accepted Date: 22 November 2024
Available Online: 23 November 2024

Figures(4)

Worsened air pollution has been linked to elevated rates of cardiovascular disease (CVD) morbidity and mortality. Atherosclerosis, a shared pathophysiological foundation for various CVD manifestations, plays a crucial role. Although foam cell formation is hypothesized to be a contributing factor, the precise mechanisms by which air pollution accelerates the advancement of atherosclerotic plaques remain unidentified. In this study, an atherosclerosis-susceptible apolipoprotein E-deficient (ApoE^−/−) mouse model was employed to examine the influence of real-world environmental PM_2.5 exposure on atherosclerosis. Metabolomic analysis was performed to identify potential biomarkers that may play a role in atherogenesis following PM_2.5 exposure. Our findings revealed that mice fed a high-cholesterol diet (HCD) exhibited susceptibility to PM_2.5 exposure, as evidenced by increased inflammation, enhanced fibrosis, and enlarged foam cell formation in the aorta. The interactive effects between PM_2.5 exposure and HCD disrupted the secretion of certain chemokines. The metabolomic data provided additional insights into how PM_2.5 exposure alters prostaglandin levels, contributing to the progression of atherosclerotic lesions. These findings enhance our understanding of the pivotal role of arachidonic acid metabolism in the etiology of PM_2.5-induced cardiovascular risks and elucidate the mechanisms by which PM_2.5 exposure leads to vascular damage in populations with high cholesterol intake.
- Air pollution,
- High-cholesterol diet,
- Cardiovascular risk,
- Metabolomics,
- Arachidonic acid metabolism
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通讯作者: 陈斌, bchen63@163.com

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沈阳化工大学材料科学与工程学院沈阳 110142

Real-world PM2.5 exposure induces prostaglandin disruption and low-density lipoprotein oxidation, exacerbating atherogenesis in ApoE−/− mice

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通讯作者: 陈斌, bchen63@163.com

Real-world PM_2.5 exposure induces prostaglandin disruption and low-density lipoprotein oxidation, exacerbating atherogenesis in ApoE^−/− mice