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Editorial
. 2022 Mar 18;130(6):848-850.
doi: 10.1161/CIRCRESAHA.122.320857. Epub 2022 Mar 17.

Autophagy in Atherosclerosis: Not All Foam Cells Are Created Equal

Gordon A Francis  1 , Babak Razani  2   3   4
Affiliations
Editorial

Autophagy in Atherosclerosis: Not All Foam Cells Are Created Equal

Gordon A Francis et al. Circ Res. .
No abstract available

Keywords: Editorials; atherosclerosis; autophagy; cholesterol; inflammation; macrophages; muscle, smooth.

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Figures

Figure 1.
Figure 1.. Diffuse intimal thickening, macrophages and smooth muscle cell foam cells in early human atherosclerosis.
A, anti-SMC actin antibody HHF35 staining of thoracic aorta in young adult male showing preponderance of SMCs in the diffusely thickened intima (I); (M), media. B, anti-macrophage antibody HAM56 of same lesion demonstrating macrophages confined largely to the immediate subendothelial region. C, Higher magnification of HHF35 staining demonstrating SMC foam cells near the base of the intima. Used with permission from reference . D, Grade 2 fatty streak in right coronary artery of a 44-year old male showing diffuse thickening in intima (I) relative to media (M). Arrowheads indicate the internal elastic lamina. E, same tissue stained with Sudan IV showing lipid staining primarily in deeper intima. F, Macrophage staining with anti-CD68. Used with permission from reference . G, Atherosclerotic plaque depicting differences between a macrophage and a SMC in the fate of hydrolyzed cholesteryl esters (CE) from uptake of modified lipids such as aggregated LDL (agLDL) or oxidized LDL (oxLDL). Free cholesterol (FC) generated by Lysosomal Acid Lipase (LAL) is re-esterified in endoplasmic reticulum (ER) by Acyl CoA Acyl Transferase (ACAT) to CE accumulating in cytosolic lipid droplets. Lipophagy then delivers these CE to lysosomes where LAL can re-hydrolyze to FC for efflux by ABCA1 or ABCG1 transporters to ApoA-I/HDL.
See this image and copyright information in PMC

Comment on

References

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