ArticleArteriosclerosis, thrombosis, and vascular biology2014
Macrophage-independent regulation of reverse cholesterol transport by liver X receptors.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Liver X receptor: A potential target for inflammatory bowel disease and colorectal cancer (Review).Molecular medicine reports · 2026Review
- A mutation in LXRα uncovers a role for cholesterol sensing in limiting metabolic dysfunction-associated steatohepatitis.Nature communications · 2025Article
- Cyclodextrin reduces cholesterol crystal uptake by circulating monocytes in patients undergoing coronary angiography.PloS one · 2025Article
- A Novel Mutation in LXRα Uncovers a Role for Cholesterol Sensing in Limiting Metabolic Dysfunction-Associated Steatohepatitis (MASH).bioRxiv : the preprint server for biology · 2024Article
- The Role of Gut Microbiota and Its Produced Metabolites in Obesity, Dyslipidemia, Adipocyte Dysfunction, and Its Interventions.Metabolites · 2021Review
- Liver X receptors and liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Molecular characterization and homology modeling of liver X receptor in Asian seabass, Lates calcarifer: predicted functions in reproduction and lipid metabolism.Fish physiology and biochemistry · 2019Article
- Therapeutic FGF19 promotes HDL biogenesis and transhepatic cholesterol efflux to prevent atherosclerosis.Journal of lipid research · 2019Article
- Structural analysis identifies an escape route from the adverse lipogenic effects of liver X receptor ligands.Communications biology · 2019Article
- Chronic Activation of Liver X Receptor Sensitizes Mice to High Cholesterol Diet-Induced Gut Toxicity.Molecular pharmacology · 2018Article
- Identfication of Potent LXRβ-Selective Agonists without LXRα Activation by In Silico Approaches.Molecules (Basel, Switzerland) · 2018Article
- Deficiency of Dab2 (Disabled Homolog 2) in Myeloid Cells Exacerbates Inflammation in Liver and Atherosclerotic Plaques in LDLR (Low-Density Lipoprotein Receptor)-Null Mice-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Liver X receptors link lipid metabolism and inflammation.FEBS letters · 2017Review
- EEPD1 Is a Novel LXR Target Gene in Macrophages Which Regulates ABCA1 Abundance and Cholesterol Efflux.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Clinically used selective estrogen receptor modulators affect different steps of macrophage-specific reverse cholesterol transport.Scientific reports · 2016Article
- Ezetimibe Promotes Brush Border Membrane-to-Lumen Cholesterol Efflux in the Small Intestine.PloS one · 2016Article
- Metabolic Flexibility and Dysfunction in Cardiovascular Cells.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Liver X receptors at the intersection of lipid metabolism and atherogenesis.Atherosclerosis · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe ability of high-density lipoprotein (HDL) particles to accept cholesterol from peripheral cells, such as lipid-laden macrophages, and to transport cholesterol to the liver for catabolism and excretion in a process termed reverse cholesterol transport (RCT) is thought to underlie the beneficial cardiovascular effects of elevated HDL. The liver X receptors (LXRs; LXRα and LXRβ) regulate RCT by controlling the efflux of cholesterol from macrophages to HDL and the excretion, catabolism, and absorption of cholesterol in the liver and intestine. Importantly, treatment with LXR agonists increases RCT and decreases atherosclerosis in animal models. Nevertheless, LXRs are expressed in multiple tissues involved in RCT, and their tissue-specific contributions to RCT are still not well defined. APPROACH AND
resultsUsing tissue-specific LXR deletions together with in vitro and in vivo assays of cholesterol efflux and fecal cholesterol excretion, we demonstrate that macrophage LXR activity is neither necessary nor sufficient for LXR agonist-stimulated RCT. In contrast, the ability of LXR agonists primarily acting in the intestine to increase HDL mass and HDL function seems to underlie the ability of LXR agonists to stimulate RCT in vivo.
conclusionsWe demonstrate that activation of LXR in macrophages makes little or no contribution to LXR agonist-stimulated RCT. Unexpectedly, our studies suggest that the ability of macrophages to efflux cholesterol to HDL in vivo is not regulated by macrophage activity but is primarily determined by the quantity and functional activity of HDL.
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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.