ArticleArteriosclerosis, thrombosis, and vascular biology2013
Molecular mechanisms responsible for the reduced expression of cholesterol transporters from macrophages by low-dose endotoxin.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Genotype-Dependent Effects of Dalcetrapib on Cholesterol Efflux and Inflammation: Concordance With Clinical Outcomes.Circulation. Cardiovascular genetics · 2016Trial
- Gut microbiota: a novel strategy affecting atherosclerosis.Microbiology spectrum · 2025Review
- Recent Advances of Trained immunity in Macrophages.International journal of biological sciences · 2025Review
- Potential Therapeutic Agents That Target ATP Binding Cassette A1 (ABCA1) Gene Expression.Drugs · 2022Review
- New insights into the emerging effects of inflammatory response on HDL particles structure and function.Molecular biology reports · 2021Review
- The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease.International journal of molecular sciences · 2021Review
- Gut Microbiota: A Novel Regulator of Cardiovascular Disease and Key Factor in the Therapeutic Effects of Flavonoids.Frontiers in pharmacology · 2021Review
- Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020Review
- Dysregulation of Lipid Metabolism in Macrophages Is Responsible for Severe Endotoxin Tolerance in FcgRIIB-Deficient Lupus Mice.Frontiers in immunology · 2020Article
- Trained Immunity: An Underlying Driver of Inflammatory Atherosclerosis.Frontiers in immunology · 2020Review
- Dietary compounds have potential in controlling atherosclerosis by modulating macrophage cholesterol metabolism and inflammation via miRNA.NPJ science of food · 2018Review
- Current and future therapies for addressing the effects of inflammation on HDL cholesterol metabolism.British journal of pharmacology · 2017Review
- Isoliquiritigenin Attenuates Atherogenesis in Apolipoprotein E-Deficient Mice.International journal of molecular sciences · 2016Article
- The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis.Nature communications · 2016Article
- Subclinical-Dose Endotoxin Sustains Low-Grade Inflammation and Exacerbates Steatohepatitis in High-Fat Diet-Fed Mice.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- The danger model: questioning an unconvincing theory.Immunology and cell biology · 2016Review
- IRAK1 mediates TLR4-induced ABCA1 downregulation and lipid accumulation in VSMCs.Cell death & disease · 2015Article
- Disruption of p21-activated kinase 1 gene diminishes atherosclerosis in apolipoprotein E-deficient mice.Nature communications · 2015Article
- Acidification of the intimal fluid: the perfect storm for atherogenesis.Journal of lipid research · 2015Review
- Role of gut microbiota in the modulation of atherosclerosis-associated immune response.Frontiers in microbiology · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAtherosclerosis is characterized as a chronic inflammatory condition that involves cholesterol deposition in arteries. Together with scavenger receptor B1 (SR-B1), the ATP-binding cassette transporters ABCA1 and ABCG1 are the major components of macrophage cholesterol efflux. Recent studies have shown that low-grade inflammation plays a distinct regulatory role in the expression of SR-B1 and ABCA1/ABCG1. However, the mechanisms linking low-grade inflammation and cholesterol accumulation are poorly understood. METHODS AND
resultsUsing primary bone-marrow-derived macrophages, we demonstrate that subclinical low-dose lipopolysaccharide potently reduces the expression of SR-B1 and ABCA1/ABCG1, as well as cholesterol efflux from macrophages through interleukin-1 receptor-associated kinase 1 and Toll-interacting-protein. Low-dose lipopolysaccharide downregulates the nuclear levels of retinoic acid receptor-α, leading to their reduced binding to the promoters of SR-B1 and ABCA1/ABCG1. We observe that glycogen synthase kinase 3β activation by low-dose lipopolysaccharide through interleukin-1 receptor-associated kinase 1 and Toll-interacting-protein is responsible for reduced levels of retinoic acid receptor-α, and reduced expression of SR-B1 and ABCA1/ABCG1. Interleukin-1 receptor-associated kinase M, however, counteracts the function of interleukin-1 receptor associated kinase 1.
conclusionsCollectively, our data reveal a novel intracellular network regulated by low-dose endotoxemia that disrupts cholesterol efflux from macrophages and leads to the pathogenesis of atherosclerosis.
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Registered trials
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.