ArticleJournal of lipid research2015
Lipoprotein (a) upregulates ABCA1 in liver cells via scavenger receptor-B1 through its oxidized phospholipids.
Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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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
14 citing papers in PubMed, 33 citations in OpenAlex.
- Effect of a PCSK9 inhibitor and a statin on cholesterol efflux capacity: A limitation of current cholesterol-lowering treatments?European journal of clinical investigation · 2022Trial
- Lipoprotein(a)-cholesterol levels estimated by vertical auto profile correlate poorly with Lp(a) mass in hyperlipidemic subjects: Implications for clinical practice interpretation of Lp(a)-mediated risk.Journal of clinical lipidologyTrial
- Review
- Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening.Atherosclerosis · 2025Article
- Dynamics of HDL-Cholesterol Following a Post-Myocardial Infarction Cardiac Rehabilitation Program.Reviews in cardiovascular medicine · 2025Article
- LDL Transcytosis by the Arterial Endothelium-Atherosclerosis by a Thousand Cuts?Current atherosclerosis reports · 2023Review
- HDL Function and Atherosclerosis: Reactive Dicarbonyls as Promising Targets of Therapy.Circulation research · 2023Review
- Approaches to Visualising Endocytosis of LDL-Related Lipoproteins.Biomolecules · 2022Review
- Apolipoprotein (a)/Lipoprotein(a)-Induced Oxidative-InflammatoryOxidative medicine and cellular longevity · 2022Article
- Proteomic Analysis of Liver from Human Lipoprotein(a) Transgenic Mice Shows an Oxidative Stress and Lipid Export Response.BioMed research international · 2018Article
- Large-Scale Analysis of Determinants, Stability, and Heritability of High-Density Lipoprotein Cholesterol Efflux Capacity.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Plasminogen promotes cholesterol efflux by the ABCA1 pathway.JCI insight · 2017Article
- Mechanistic insights into Lp(a)-induced IL-8 expression: a role for oxidized phospholipid modification of apo(a).Journal of lipid research · 2015Article
- HDL-C, ABCA1-mediated cholesterol efflux, and lipoprotein(a): insights into a potential novel physiologic role of lipoprotein(a).Journal of lipid research · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated levels of lipoprotein (a) [Lp(a)] are a well-established risk factor for developing CVD. While Lp(a) levels are thought to be independent of other plasma lipoproteins, some trials have reported a positive association between Lp(a) and HDL. Whether Lp(a) has a direct effect on HDL is not known. Here we investigated to determine whether Lp(a) had any effect on the ABCA1 pathway of HDL production in liver cells. Incubation of HepG2 cells with Lp(a) upregulated the PPARγ protein by 1.7-fold and the liver X receptor α protein by 3-fold. This was accompanied by a 1.8-fold increase in ABCA1 protein and a 1.5-fold increase in cholesterol efflux onto apoA1. We showed that Lp(a) was internalized by HepG2 cells, however, the ABCA1 response to Lp(a) was mediated by the selective uptake of oxidized phospholipids (oxPLs) from Lp(a) via the scavenger receptor-B1 and not by Lp(a) internalization per se. We conclude that there is a biological connection between Lp(a) and HDL through the ability of Lp(a)'s oxPLs to upregulate HDL biosynthesis.
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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.