ArticleThe Journal of biological chemistry2016
Myeloid Acyl-CoA:Cholesterol Acyltransferase 1 Deficiency Reduces Lesion Macrophage Content and Suppresses Atherosclerosis Progression.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Temporal Dynamics of CNS Cholesterol Esters Correlate with Demyelination and Remyelination.ACS chemical neuroscience · 2026Article
- Temporal dynamics of CNS cholesterol esters correlate with demyelination and remyelination.bioRxiv : the preprint server for biology · 2025Article
- Targeting Regulation of Macrophage to Treat Metabolic Disease: Role of Phytochemicals.Cell proliferation · 2025Review
- Understanding the Link Between Sterol Regulatory Element Binding Protein (SREBPs) and Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).Current obesity reports · 2025Review
- ACAT1/SOAT1 Blockade Suppresses LPS-Mediated Neuroinflammation by Modulating the Fate of Toll-like Receptor 4 in Microglia.International journal of molecular sciences · 2023Article
- Monocyte and macrophage foam cells in diabetes-accelerated atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- Regulation of cholesterol homeostasis in health and diseases: from mechanisms to targeted therapeutics.Signal transduction and targeted therapy · 2022Review
- Article
- Pinocytotic engulfment of lipoproteins by macrophages.Frontiers in cardiovascular medicine · 2022Review
- Acyl-Coenzyme A: Cholesterol Acyltransferase (ACAT) in Cholesterol Metabolism: From Its Discovery to Clinical Trials and the Genomics Era.Metabolites · 2021Review
- Cholesterol, Atherosclerosis, and APOE in Vascular Contributions to Cognitive Impairment and Dementia (VCID): Potential Mechanisms and Therapy.Frontiers in aging neuroscience · 2021Article
- Soat1 mediates the mouse strain effects on cholesterol loading-induced endoplasmic reticulum stress and CHOP expression in macrophages.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021Article
- Sterol-O-acyltransferase-1 has a role in kidney disease associated with diabetes and Alport syndrome.Kidney international · 2020Article
- Article
- Sex as a Biological Variable in Atherosclerosis.Circulation research · 2020Review
- MyeloidThe Journal of biological chemistry · 2019Article
- Loss of ACAT1 Attenuates Atherosclerosis Aggravated by Loss of NCEH1 in Bone Marrow-Derived Cells.Journal of atherosclerosis and thrombosis · 2019Article
- Myeloid-specific Acat1 ablation attenuates inflammatory responses in macrophages, improves insulin sensitivity, and suppresses diet-induced obesity.American journal of physiology. Endocrinology and metabolism · 2018Article
- Cholesterol and bile acid-mediated regulation of autophagy in fatty liver diseases and atherosclerosis.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Review
- In vitro exploration of ACAT contributions to lipid droplet formation during adipogenesis.Journal of lipid research · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Acyl-CoA:cholesterol acyltransferase 1 (Acat1) converts cellular cholesterol to cholesteryl esters and is considered a drug target for treating atherosclerosis. However, in mouse models for atherosclerosis, global Acat1 knockout (Acat1(-/-)) did not prevent lesion development. Acat1(-/-) increased apoptosis within lesions and led to several additional undesirable phenotypes, including hair loss, dry eye, leukocytosis, xanthomatosis, and a reduced life span. To determine the roles of Acat1 in monocytes/macrophages in atherosclerosis, we produced a myeloid-specific Acat1 knockout (Acat1(-M/-M)) mouse and showed that, in the Apoe knockout (Apoe(-/-)) mouse model for atherosclerosis, Acat1(-M/-M) decreased the plaque area and reduced lesion size without causing leukocytosis, dry eye, hair loss, or a reduced life span. Acat1(-M/-M) enhanced xanthomatosis in apoe(-/-) mice, a skin disease that is not associated with diet-induced atherosclerosis in humans. Analyses of atherosclerotic lesions showed that Acat1(-M/-M) reduced macrophage numbers and diminished the cholesterol and cholesteryl ester load without causing detectable apoptotic cell death. Leukocyte migration analysis in vivo showed that Acat1(-M/-M) caused much fewer leukocytes to appear at the activated endothelium. Studies in inflammatory (Ly6C(hi)-positive) monocytes and in cultured macrophages showed that inhibiting ACAT1 by gene knockout or by pharmacological inhibition caused a significant decrease in integrin β 1 (CD29) expression in activated monocytes/macrophages. The sparse presence of lesion macrophages without Acat1 can therefore, in part, be attributed to decreased interaction between inflammatory monocytes/macrophages lacking Acat1 and the activated endothelium. We conclude that targeting ACAT1 in a myeloid cell lineage suppresses atherosclerosis progression while avoiding many of the undesirable side effects caused by global Acat1 inhibition.
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Registered trials
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