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

<jats:title>Abstract</jats:title><jats:p>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 (PM<jats:sub>2.5</jats:sub>) plays a major mortality risk factor particularly on cardiovascular diseases through mechanisms of atherosclerosis, thrombosis and inflammation. A review on the PM<jats:sub>2.5</jats:sub>-induced atherosclerosis is needed to better understand the involved mechanisms. In this review, we summarized epidemiology and animal studies of PM<jats:sub>2.5</jats:sub>-induced atherosclerosis. Vascular endothelial injury is a critical early predictor of atherosclerosis. The evidence of mechanisms of PM<jats:sub>2.5</jats:sub>-induced atherosclerosis supports effects on vascular function. Thus, we summarized the main mechanisms of PM<jats:sub>2.5</jats:sub>-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 PM<jats:sub>2.5</jats:sub>-induced endothelial injury and atherosclerosis. PM<jats:sub>2.5</jats:sub>-induced endothelial injury associated with inflammation, pro-coagulation and lipid deposition. Although the evidence of PM<jats:sub>2.5</jats:sub>-induced atherosclerosis is undergoing continual refinement, the mechanisms of PM<jats:sub>2.5</jats:sub>-triggered atherosclerosis are still limited, especially indoor PM<jats:sub>2.5</jats:sub>. Subsequent efforts of researchers are needed to improve the understanding of PM<jats:sub>2.5</jats:sub> and atherosclerosis. Preventing or avoiding PM<jats:sub>2.5</jats:sub>-induced endothelial damage may greatly reduce the occurrence and development of atherosclerosis.</jats:p>