Evidence map›Paper›PMID 35053320›Full record

ArticleCells2022

Native and Oxidized Low-Density Lipoproteins Increase the Expression of the LDL Receptor and the LOX-1 Receptor, Respectively, in Arterial Endothelial Cells.

Rusan Catar, Lei Chen, Hongfan Zhao, Dashan Wu, Julian Kamhieh-Milz, Christian Lücht, Daniel Zickler, Alexander W Krug, Christian G Ziegler, Henning Morawietz and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  4. Protective Effect ofJournal of microbiology and biotechnology · 2025
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  7. Ginsenoside RbChinese herbal medicines · 2024
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  8. Review
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  10. Review
  11. Article
  12. Cross-Talk of NADPH Oxidases and Inflammation in Obesity.Antioxidants (Basel, Switzerland) · 2023
    Review
  13. Article
  14. Review
  15. The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Rusan CatarDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0002-7000-7860
Lei ChenDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Hongfan ZhaoDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0001-8938-6867
Dashan WuDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Julian Kamhieh-MilzInstitute of Transfusion Medicine, Charité Universitätsmedizin Berlin, 10117 Berlin, Germany.
Christian LüchtDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Daniel ZicklerDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Alexander W KrugDepartment of Medicine III, University Hospital Carl Gustav Carus Dresden, 01307 Dresden, Germany.
Christian G ZieglerDepartment of Medicine III, University Hospital Carl Gustav Carus Dresden, 01307 Dresden, Germany.
Henning MorawietzDepartment of Medicine III, Division of Vascular Endothelium and Microcirculation, University Hospital Carl Gustav Carus Dresden, Technische Universität Dresden, Fetscherstr. 74, 01307 Dresden, Germany.ORCID 0000-0001-9360-9736
Janusz WitowskiDepartment of Nephrology and Internal Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0002-1093-6027
Humboldt-Universität zu Berlin · DEUniversity Hospital Carl Gustav Carus · DECharité - Universitätsmedizin Berlin · DEPoznan University of Medical Sciences · PL

Funding

Deutsche Forschungsgemeinschaft 394046635
6 · The paper itself

Abstract

Atherosclerotic artery disease is the major cause of death and an immense burden on healthcare systems worldwide. The formation of atherosclerotic plaques is promoted by high levels of low-density lipoproteins (LDL) in the blood, especially in the oxidized form. Circulating LDL is taken up by conventional and non-classical endothelial cell receptors and deposited in the vessel wall. The exact mechanism of LDL interaction with vascular endothelial cells is not fully understood. Moreover, it appears to depend on the type and location of the vessel affected and the receptor involved. Here, we analyze how native LDL (nLDL) and oxidized LDL (oxLDL) modulate the expression of their receptors-classical LDLR and alternative LOX-1-in endothelial cells derived from human umbilical artery (HUAECs), used as an example of a medium-sized vessel, which is typically affected by atherosclerosis. Exposure of HUAECs to nLDL resulted in moderate nLDL uptake and gradual increase in LDLR, but not LOX-1, expression over 24 h. Conversely, exposure of HUAECs to oxLDL, led to significant accumulation of oxLDL and rapid induction of LOX-1, but not LDLR, within 7 h. These activation processes were associated with phosphorylation of protein kinases ERK1/2 and p38, followed by activation of the transcription factor AP-1 and its binding to the promoters of the respective receptor genes. Both nLDL-induced

Indexed as

Gene Expression RegulationCells, CulturedCell SurvivalEndothelial CellsEnzyme ActivationHumansLipoproteins, LDLMAP Kinase Signaling SystemNF-kappa BOxidation-Reductionp38 Mitogen-Activated Protein KinasesPromoter Regions, GeneticReceptors, LDLScavenger Receptors, Class ETranscription Factor AP-1Umbilical ArteriesLipoproteins, LDLNF-kappa BOLR1 protein, humanoxidized low density lipoproteinp38 Mitogen-Activated Protein KinasesReceptors, LDLScavenger Receptors, Class ETranscription Factor AP-1AP-1atherosclerosisendotheliumLDLLDL receptorLOX-1NF-κB

Identifiers

PMID35053320
PMCPMC8774144
OpenAlexW4206180611

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.