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

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.

Ambient Particulate Matter Induces Vascular Smooth Muscle Cell Phenotypic Changes via NOX1/ROS/NF-κB Dependent and Independent Pathways: Protective Effects of Polyphenols

“…Atherosclerosis is one of the major vascular diseases induced by PM 2.5 . More recently, Liang et al [ 62 ] indicated that vascular endothelial injury plays a critical role in PM 2.5 -trigered atherosclerosis. Endothelial cells consist of a single layer of the tunica intima.…”

“…On the other hand, VSMCs in the tunica media may respond to the signals of injured endothelial cells and switch to highly migratory and proliferative phenotypes [ 63 ]. Liang et al [ 62 ] pointed out that oxidative stress induced by PM 2.5 can increase VSMCs proliferation. Our present study further demonstrated that oxidative stress induced by PM 2.5 increased VMSCs migration.…”

Activation of the Complement System on Human Endothelial Cells by Urban Particulate Matter Triggers Inflammation-Related Protein Production

“…To the best of our knowledge, there are no methods available for measuring the level of PM in blood vessels due to a lack of measuring tools and the sparse concentration of PM in blood. Therefore, we determined PM concentrations in this study using the PM concentrations applied in previous studies targeting vascular endothelial cells [ 40 ].…”

Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

“…PM can exert proarrhythmic effects indirectly that are mediated through the systemic inflammatory responses (38)(39)(40). Systemic inflammation is known to contribute to the progression of atherosclerosis (41), resulting in chronic and acute ischemia. Ischemic heart disease leads to ion channel remodeling, augments spatial dispersion of depolarization, thereby providing substrates for cardiac arrhythmias (42,43).…”