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.