ArticleThe Journal of clinical investigation2021
Eruptive xanthoma model reveals endothelial cells internalize and metabolize chylomicrons, leading to extravascular triglyceride accumulation.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- The N-terminus of apolipoprotein B mediates the interaction of atherogenic lipoproteins with endothelial cells.The Journal of clinical investigation · 2026Article
- GPR182 is a lipoprotein receptor for dietary fat absorption.The Journal of clinical investigation · 2026Article
- Kidney-Vascular Metabolic Crosstalk: Altered Lipoproteins in CKD.Circulation research · 2026Review
- Triglyceride-Rich Lipoprotein Metabolism and Cardiovascular Risk in Diabetes: Bedside to Bench to Bedside.Circulation research · 2026Review
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Endothelial Cell Regulation of Lipid Uptake During Feeding and Fasting.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Non-remnant triglyceride-rich lipoproteins due to lipoprotein lipase deficiency increase atherosclerosis in mice.Nature communications · 2026Article
- Extracellular Vesicles From Chylomicron-Treated Endothelial Cells Drive Macrophage Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Apolipoprotein B-containing lipoproteins in atherogenesis.Nature reviews. Cardiology · 2025Review
- Distinct roles of size-defined HDL subpopulations in cardiovascular disease.Current opinion in lipidology · 2025Review
- Atherosclerosis: from lipid-lowering and anti-inflammatory therapies to targeting arterial retention of ApoB-containing lipoproteins.Frontiers in immunology · 2025Review
- Imbalance of APOB Lipoproteins and Large HDL in Type 1 Diabetes Drives Atherosclerosis.Circulation research · 2024Article
- In the Beginning, Lipoproteins Cross the Endothelial Barrier.Journal of atherosclerosis and thrombosis · 2024Review
- Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice.The Journal of clinical investigation · 2024Article
- Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study.European heart journal · 2023Article
- Article
- Fatty Acid Transport and Signaling: Mechanisms and Physiological Implications.Annual review of physiology · 2023Review
- Lysosomal acid lipase promotes endothelial proliferation in cold-activated adipose tissue.Adipocyte · 2022Article
- Novel pathogenic variant combination inTranslational pediatrics · 2022Article
- Endothelial Lipid Metabolism.Cold Spring Harbor perspectives in medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Although tissue uptake of fatty acids from chylomicrons is primarily via lipoprotein lipase (LpL) hydrolysis of triglycerides (TGs), studies of patients with genetic LpL deficiency suggest additional pathways deliver dietary lipids to tissues. Despite an intact endothelial cell (EC) barrier, hyperchylomicronemic patients accumulate chylomicron-derived lipids within skin macrophages, leading to the clinical finding eruptive xanthomas. We explored whether an LpL-independent pathway exists for transfer of circulating lipids across the EC barrier. We found that LpL-deficient mice had a marked increase in aortic EC lipid droplets before and after a fat gavage. Cultured ECs internalized chylomicrons, which were hydrolyzed within lysosomes. The products of this hydrolysis fueled lipid droplet biogenesis in ECs and triggered lipid accumulation in cocultured macrophages. EC chylomicron uptake was inhibited by competition with HDL and knockdown of the scavenger receptor-BI (SR-BI). In vivo, SR-BI knockdown reduced TG accumulation in aortic ECs and skin macrophages of LpL-deficient mice. Thus, ECs internalize chylomicrons, metabolize them in lysosomes, and either store or release their lipids. This latter process may allow accumulation of TGs within skin macrophages and illustrates a pathway that might be responsible for creation of eruptive xanthomas.
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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.