ArticleMolecular medicine (Cambridge, Mass.)2022
The LOX-1 receptor ectopically expressed in the liver alleviates atherosclerosis by clearing Ox-LDL from the circulation.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Endothelial cell LGR4 maintains liver sinusoidal endothelial cell Identity and protects against hepatic steatosis.Life sciences · 2026Article
- Ischemic preconditioning promotes hepatic differentiation in human liver organoids.Frontiers in cell and developmental biology · 2026Article
- The Connection Between Lipid Metabolism in the Heart and Liver of Wuzhishan Pigs.Biomolecules · 2025Article
- PPP2CB aggravates atherosclerosis-related dyslipidemia via LOX-1/MAPK/ERK signaling pathway.Lipids in health and disease · 2025Article
- Effect of Propolis Extracts on OxLDL and LOX-1 Levels in ApoE Knockout Mice Fed a High Fat Diet.Life (Basel, Switzerland) · 2025Article
- HADHA Regulates Respiratory Complex Assembly and Couples FAO and OXPHOS.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Research Progress on the Pathogenesis and Treatment of Neoatherosclerosis.Current medical science · 2024Review
- Ellagic acid, a functional food component, ameliorates functionality of reverse cholesterol transport in murine model of atherosclerosis.Nutrition research and practice · 2024Article
- Chromium Nanoparticles Together with a Switch Away from High-Fat/Low-Fiber Dietary Habits Enhances the Pro-Healthy Regulation of Liver Lipid Metabolism and Inflammation in Obese Rats.International journal of molecular sciences · 2023Article
- GAS1 Promotes Ferroptosis of Liver Cells in Acetaminophen-Induced Acute Liver Failure.International journal of medical sciences · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOxidized Low-Density-Lipoprotein (Ox-LDL) is the core factor in the development of atherosclerosis. However, there are few therapies aimed at eliminating Ox-LDL. Here in this study, we investigate whether the ectopically expression of the lectin-like oxidized low density lipoprotein receptor (LOX-1) in the liver could lead to the elimination of circulating Ox-LDL and prevent the deposition in the vascular wall, thereby alleviating the progression of atherosclerosis.
methodsApolipoprotein E-deficient (ApoE
resultsThe expression of LOX-1 was stable in liver within 4 weeks. Ectopically expressed LOX-1 in the liver phagocytosed and degraded Ox-LDL and reduced Ox-LDL from circulation but did not have a significant effect on blood lipid levels. After the expression of LOX-1 in liver, Ox-LDL can be cleared by the hepatocytes, thereby reducing VCAM-1 expression in vascular endothelium and the migration of macrophages in plaques, and eventually alleviating the progression of atherosclerosis. Functional expression of LOX-1 in hepatocytes may facilitate the metabolic clearance of Ox-LDL by upregulating the expression of ATP-binding cassette G5 and G8 (ABCG5/G8), which is the primary neutral sterol transporter in hepatobiliary and transintestinal cholesterol excretion.
conclusionEctopic liver-specific expression of LOX-1 receptor alleviates the progression of atherosclerosis by clearing Ox-LDL from circulation.
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