Fig. 1
From: The critical role of endothelial function in fine particulate matter-induced atherosclerosis
Summarized the main pathogenic mechanisms of PM2.5-triggered atherosclerosis. Four main hypotheses have proposed by which inhaled particulate matter effect on cardiovascular system [49]: a. inflammatory mediators; b. unidentified mediators; c. autonomic imbalance; d. direct particle translocation. PM2.5 increased endothelial permeability, declined vascular tone and vascular reparative capacity, thus induced vascular endothelial injury. The initial step of atherosclerosis is vascular endothelial dysfunction, and then activated endothelial cells promoted monocytes recruited and maturation of monocytes into macrophages. Lipid accumulation and continued uptake by macrophages lead to foam cell formation and then developed into atherosclerotic lesion