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

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_2.5) plays a major mortality risk factor particularly on cardiovascular diseases through mechanisms of atherosclerosis, thrombosis and inflammation. A review on the PM_2.5-induced atherosclerosis is needed to better understand the involved mechanisms. In this review, we summarized epidemiology and animal studies of PM_2.5-induced atherosclerosis. Vascular endothelial injury is a critical early predictor of atherosclerosis. The evidence of mechanisms of PM_2.5-induced atherosclerosis supports effects on vascular function. Thus, we summarized the main mechanisms of PM_2.5-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 PM_2.5-induced endothelial injury and atherosclerosis. PM_2.5-induced endothelial injury associated with inflammation, pro-coagulation and lipid deposition. Although the evidence of PM_2.5-induced atherosclerosis is undergoing continual refinement, the mechanisms of PM_2.5-triggered atherosclerosis are still limited, especially indoor PM_2.5. Subsequent efforts of researchers are needed to improve the understanding of PM_2.5 and atherosclerosis. Preventing or avoiding PM_2.5-induced endothelial damage may greatly reduce the occurrence and development of atherosclerosis.