PM2.5 promotes plaque vulnerability at different stages of atherosclerosis and the formation of foam cells via TLR4/MyD88/NFκB pathway.
Air Pollution
/ adverse effects
Animals
Apolipoproteins E
/ metabolism
Atherosclerosis
/ pathology
CD36 Antigens
/ metabolism
Foam Cells
/ drug effects
Macrophages
/ drug effects
Mice
Myeloid Differentiation Factor 88
/ metabolism
Myocytes, Smooth Muscle
/ drug effects
NF-kappa B
/ metabolism
Particle Size
Particulate Matter
/ chemistry
Plaque, Atherosclerotic
/ metabolism
Toll-Like Receptor 4
/ metabolism
Atherosclerosis
Foam cell
PM2.5
Plaque vulnerability
TLR4
Journal
Ecotoxicology and environmental safety
ISSN: 1090-2414
Titre abrégé: Ecotoxicol Environ Saf
Pays: Netherlands
ID NLM: 7805381
Informations de publication
Date de publication:
30 Jul 2019
30 Jul 2019
Historique:
received:
29
09
2018
revised:
09
03
2019
accepted:
15
03
2019
pubmed:
29
3
2019
medline:
18
6
2019
entrez:
29
3
2019
Statut:
ppublish
Résumé
Clinical evidence has shown an elevated myocardial infarction (MI) risk after PM2.5 (particulate matter < 2.5 μm) exposure. Incident MI may result from rupture of vulnerable plaques. To test whether PM2.5 could promote plaque vulnerability, we exposed PM2.5 to apoe
Identifiants
pubmed: 30921699
pii: S0147-6513(19)30329-X
doi: 10.1016/j.ecoenv.2019.03.068
pii:
doi:
Substances chimiques
Apolipoproteins E
0
CD36 Antigens
0
Myeloid Differentiation Factor 88
0
NF-kappa B
0
Particulate Matter
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
76-84Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.