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Inhibition of acyl-coenzyme A:cholesterol acyltransferase stimulates cholesterol efflux from macrophages and stimulates farnesoid X receptor in hepatocytes

An, Sojin, Jang, Young-Soon, Park, Ji-Seon, Kwon, Byoung-Mog, Paik, Young-Ki, Jeong, Tae-Sook·2008·Experimental and Molecular Medicine
DOI 10.3858/emm.2008.40.4.407
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  • Inhibiting ACAT increases the free cholesterol pool and facilitates lipid secretion to extracellular apoE-containing lipoproteins.

    “Thus, inhibiting ACAT increases the FC pool and facilitates lipid secretion to extracellular apoE-containing lipoproteins.”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [61]

    In 'Decrement of CE mass dominates the negative effect of the accumulation of FC' (page unavailable), ACAT inhibition increased cellular free cholesterol and its secretion into the medium in acLDL-loaded THP-1 macrophages. The paper does not show that the secreted lipid entered extracellular apoE-containing lipoproteins; 'ACAT inhibition triggers changes in expression of genes involved in cholesterol catabolism and mobilization' instead reports that Apoe mRNA was unaffected. (LLM, conf=0.88)

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  • The decrease in endothelial cell disruption and atherosclerotic plaque development was dependent on apoA1 as the plasma cholesterol acceptor.

    “This decrease in endothelial cell disruption and atherosclerotic plaque development was dependent on apoA1 as the plasma cholesterol acceptor [57–63].”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [61]

    The Introduction and Discussion (page unavailable) discuss cholesterol efflux from macrophages and a possible benefit for atherosclerosis, but do not report a decrease in endothelial disruption or plaque development. The cholesterol-efflux assay describes no apoA1-dependent test; searches for apoA1, cholesterol acceptors, endothelial cells, and plaques found no passage establishing the claimed dependence. (LLM, conf=0.77)

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Metadata

Authors
An, S., Jang, Y.-S., Park, J.-S., Kwon, B.-M., Paik, Y.-K., & Jeong, T.-S.
Affiliations
  • National Research Laboratory of Lipid Metabolism and Atherosclerosis, KRIBB, Daejeon 305-806, Korea.
  • Therapeutic Antibody Research Center, KRIBB, Daejeon 305-806, Korea.
  • Molecular Cancer Research Center, KRIBB, Daejeon 305-806, Korea.
  • Department of Biochemistry, Yonsei University, Seoul 131-749, Korea.
Venue
Experimental and Molecular Medicine
Publisher
Springer Science and Business Media LLC
Published
2008
Volume
40
Issue
4
Pages
407
ISSN
1226-3613
DOI
10.3858/emm.2008.40.4.407
Cited by
19
References
2
Language
en

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