The critical role of endothelial function in fine particulate matter-induced atherosclerosis

• Main Authors: Shuang Liang, Jingyi Zhang, Ruihong Ning, Zhou Du, Jiangyan Liu, Joe Werelagi Batibawa, Junchao Duan, Zhiwei Sun
• Format: Article
• Language: English
• Published: BMC 2020-12-01
• Series: Particle and Fibre Toxicology
• Subjects: PM2.5; Endothelial dysfunction; Inflammation; Coagulation; Lipid deposition; Atherosclerosis
• Online Access: https://doi.org/10.1186/s12989-020-00391-x

Abstract Ambient and indoor air pollution contributes annually to approximately seven million premature deaths. Air pollution is a complex mixture of gaseous and particulate materials. In particular, fine particulate matter (PM2.5) plays a major mortality risk factor particularly on cardiovascular diseases through mechanisms of atherosclerosis, thrombosis and inflammation. A review on the PM2.5-induced atherosclerosis is needed to better understand the involved mechanisms. In this review, we summarized epidemiology and animal studies of PM2.5-induced atherosclerosis. Vascular endothelial injury is a critical early predictor of atherosclerosis. The evidence of mechanisms of PM2.5-induced atherosclerosis supports effects on vascular function. Thus, we summarized the main mechanisms of PM2.5-triggered vascular endothelial injury, which mainly involved three aspects, including vascular endothelial permeability, vasomotor function and vascular reparative capacity. Then we reviewed the relationship between PM2.5-induced endothelial injury and atherosclerosis. PM2.5-induced endothelial injury associated with inflammation, pro-coagulation and lipid deposition. Although the evidence of PM2.5-induced atherosclerosis is undergoing continual refinement, the mechanisms of PM2.5-triggered atherosclerosis are still limited, especially indoor PM2.5. Subsequent efforts of researchers are needed to improve the understanding of PM2.5 and atherosclerosis. Preventing or avoiding PM2.5-induced endothelial damage may greatly reduce the occurrence and development of atherosclerosis.