Macrophage foam cells and atherosclerosis

10.2741/kruth ◽  
2001 ◽  
Vol 6 (1) ◽  
pp. d429 ◽  
Author(s):  
Howard, S. Kruth
Keyword(s):  
Foam Cells ◽  
Macrophage Foam Cells

scholarly journals Lysosomal accumulation of unesterified cholesterol in model macrophage foam cells

1993 ◽  
Vol 268 (13) ◽  
pp. 9653-9660
Author(s):  
R.K. Tangirala ◽  
F.H. Mahlberg ◽  
J.M. Glick ◽  
W.G. Jerome ◽  
G.H. Rothblat
Keyword(s):  
Foam Cells ◽  
Unesterified Cholesterol ◽  
Macrophage Foam Cells ◽  
Lysosomal Accumulation

Identification of novel lipid droplet factors that regulate autophagy and cholesterol efflux in macrophage foam cells

2021 ◽  
Vol 331 ◽  
pp. e2
Author(s):  
S. Robichaud ◽  
G. Fairman ◽  
V. Vijithakumar ◽  
E. Mak ◽  
D. Cook ◽  
...  
Keyword(s):  
Lipid Droplet ◽  
Cholesterol Efflux ◽  
Foam Cells ◽  
Macrophage Foam Cells

scholarly journals Cholesterol Acceptors Regulate the Lipidome of Macrophage Foam Cells

2019 ◽  
Vol 20 (15) ◽  
pp. 3784 ◽  
Author(s):  
Antoni Paul ◽  
Todd A. Lydic ◽  
Ryan Hogan ◽  
Young-Hwa Goo
Keyword(s):  
High Density Lipoprotein ◽  
Free Cholesterol ◽  
Foam Cell ◽  
Density Lipoprotein ◽  
Foam Cells ◽  
Atherosclerotic Plaques ◽  
Plaque Instability ◽  
Apolipoprotein A ◽  
Lipid Species ◽  
Macrophage Foam Cells

Arterial foam cells are central players of atherogenesis. Cholesterol acceptors, apolipoprotein A-I (apoA-I) and high-density lipoprotein (HDL), take up cholesterol and phospholipids effluxed from foam cells into the circulation. Due to the high abundance of cholesterol in foam cells, most previous studies focused on apoA-I/HDL-mediated free cholesterol (FC) transport. However, recent lipidomics of human atherosclerotic plaques also identified that oxidized sterols (oxysterols) and non-sterol lipid species accumulate as atherogenesis progresses. While it is known that these lipids regulate expression of pro-inflammatory genes linked to plaque instability, how cholesterol acceptors impact the foam cell lipidome, particularly oxysterols and non-sterol lipids, remains unexplored. Using lipidomics analyses, we found cholesterol acceptors remodel foam cell lipidomes. Lipid subclass analyses revealed various oxysterols, sphingomyelins, and ceramides, species uniquely enriched in human plaques were significantly reduced by cholesterol acceptors, especially by apoA-I. These results indicate that the function of lipid-poor apoA-I is not limited to the efflux of cholesterol and phospholipids but suggest that apoA-I serves as a major regulator of the foam cell lipidome and might play an important role in reducing multiple lipid species involved in the pathogenesis of atherosclerosis.

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