ArticleCirculation research2014
Cholesterol esters (CE) derived from hepatic sterol O-acyltransferase 2 (SOAT2) are associated with more atherosclerosis than CE from intestinal SOAT2.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Dyslipidaemia and hepatic steatosis: mechanisms and implications for lipid-lowering therapy.Nature reviews. Cardiology · 2026Review
- Novel molecular mechanisms of immune evasion in hepatocellular carcinoma: NSUN2-mediated increase of SOAT2 RNA methylation.Cancer communications (London, England) · 2025Article
- From Genetic Findings to new Intestinal Molecular Targets in Lipid Metabolism.Current atherosclerosis reports · 2025Review
- Physiological Effects of Soat1 Inactivation on Homeostasis of the Mouse Ocular Surface.Investigative ophthalmology & visual science · 2024Article
- Insights Into Long Non-Coding RNA and mRNA Expression in the Jejunum of Lambs Challenged WithFrontiers in veterinary science · 2022Article
- Genetic architecture and major genes for backfat thickness in pig lines of diverse genetic backgrounds.Genetics, selection, evolution : GSE · 2021Article
- Combined Lipidomics and Network Pharmacology Study of Protective Effects ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Small molecule inhibition of gut microbial choline trimethylamine lyase activity alters host cholesterol and bile acid metabolism.American journal of physiology. Heart and circulatory physiology · 2020Article
- Ontogenesis and Modulation of Intestinal Unesterified Cholesterol Sequestration in a Mouse Model of Niemann-Pick C1 Disease.Digestive diseases and sciences · 2020Article
- Transcriptome and miRNome Analysis Provide New Insight Into Host Lipid Accumulation, Innate Immunity, and Viral Persistence in Hepatitis C Virus InfectionFrontiers in microbiology · 2020Article
- Resveratrol inhibits lipid accumulation in the intestine of atherosclerotic mice and macrophages.Journal of cellular and molecular medicine · 2019Article
- Acyl-CoA: cholesterol acyltransferases-2 gene polymorphism is associated with increased susceptibility to coronary artery disease in Uygur population in Xinjiang, China.Bioscience reports · 2019Article
- Impact of loss of SOAT2 function on disease progression in the lysosomal acid lipase-deficient mouse.Steroids · 2018Article
- Article
- Shunts, channels and lipoprotein endosomal traffic: a new model of cholesterol homeostasis in the hepatocyte.Journal of biomedical research · 2017Article
- Article
- Sterol O-Acyltransferase 2 Contributes to the Yolk Cholesterol Trafficking during Zebrafish Embryogenesis.PloS one · 2016Article
- New pyripyropene A derivatives, highly SOAT2-selective inhibitors, improve hypercholesterolemia and atherosclerosis in atherogenic mouse models.The Journal of pharmacology and experimental therapeutics · 2015Article
- Targeted Knockdown of Hepatic SOAT2 With Antisense Oligonucleotides Stabilizes Atherosclerotic Plaque in ApoB100-only LDLr-/- Mice.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Deletion of sterol O-acyltransferase 2 (SOAT2) function in mice deficient in lysosomal acid lipase (LAL) dramatically reduces esterified cholesterol sequestration in the small intestine and liver.Biochemical and biophysical research communications · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
rationaleCholesterol esters (CE), especially cholesterol oleate, generated by hepatic and intestinal sterol O-acyltransferase 2 (SOAT2) play a critical role in cholesterol homeostasis. However, it is unknown whether the contribution of intestine-derived CE from SOAT2 would have similar effects in promoting atherosclerosis progression as for liver-derived CE.
objectiveTo test whether, in low-density lipoprotein receptor null (LDLr(-/-)) mice, the conditional knockout of intestinal SOAT2 (SOAT2(SI-/SI-)) or hepatic SOAT2 (SOAT2(L-/L-)) would equally limit atherosclerosis development compared with the global deletion of SOAT2 (SOAT2(-/-)). METHODS AND
resultsSOAT2 conditional knockout mice were bred with LDLr(-/-) mice creating LDLr(-/-) mice with each of the specific SOAT2 gene deletions. All mice then were fed an atherogenic diet for 16 weeks. SOAT2(SI-/SI-)LDLr(-/-) and SOAT2(-/-)LDLr(-/-) mice had significantly lower levels of intestinal cholesterol absorption, more fecal sterol excretion, and lower biliary cholesterol levels. Analysis of plasma LDL showed that all mice with SOAT2 gene deletions had LDL CE with reduced percentages of cholesterol palmitate and cholesterol oleate. Each of the LDLr(-/-) mice with SOAT2 gene deletions had lower accumulations of total cholesterol and CE in the liver compared with control mice. Finally, aortic atherosclerosis development was significantly lower in all mice with global or tissue-restricted SOAT2 gene deletions. Nevertheless, SOAT2(-/-)LDLr(-/-) and SOAT2(L-/L-)LDLr(-/-) mice had less aortic CE accumulation and smaller aortic lesions than SOAT2(SI-/SI-)LDLr(-/-) mice.
conclusionsSOAT2-derived CE from both the intestine and liver significantly contribute to the development of atherosclerosis, although the CE from the hepatic enzyme appeared to promote more atherosclerosis development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.