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HERO ID
7497136
Reference Type
Journal Article
Subtype
Review
Title
The critical role of endothelial function in fine particulate matter-induced atherosclerosis
Author(s)
Liang, S; Zhang, J; Ning, R; Du, Z; Liu, J; Batibawa, JW; Duan, J; Sun, Z
Year
2020
Is Peer Reviewed?
1
Journal
Particle and Fibre Toxicology
EISSN:
1743-8977
Volume
17
Issue
1
Page Numbers
61
Language
English
PMID
33276797
DOI
10.1186/s12989-020-00391-x
Web of Science Id
WOS:000595742600001
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.
Keywords
PM2.5; Endothelial dysfunction; Inflammation; Coagulation; Lipid deposition; Atherosclerosis
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