Evidence map›Paper›PMID 35269979›Full record

ArticleInternational journal of molecular sciences2022

Myeloperoxidase-Oxidized LDL Activates Human Aortic Endothelial Cells through the LOX-1 Scavenger Receptor.

Layal El-Hajjar, Judy Hindieh, Rana Andraos, Marwan El-Sabban, Jalil Daher

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 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
2.0field-weighted citation impact, top 13% 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, 26 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
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  5. Review
  6. Association of Copper with Atherosclerosis and Treatment Strategies.Journal of cardiovascular translational research · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. TheInnate immunity · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Halogenation Activity of Mammalian Heme Peroxidases.Antioxidants (Basel, Switzerland) · 2022
    Review
  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

5 authors at 2 institutions in 1 country.

Layal El-HajjarDepartment of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut 1107 2020, Lebanon.ORCID 0000-0003-3123-5577
Judy HindiehDepartment of Biology, Faculty of Arts and Sciences, University of Balamand, Kalhat, Tripoli P.O. Box 100, Lebanon.
Rana AndraosDepartment of Biology, Faculty of Arts and Sciences, University of Balamand, Kalhat, Tripoli P.O. Box 100, Lebanon.
Marwan El-SabbanDepartment of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut 1107 2020, Lebanon.
Jalil DaherDepartment of Biology, Faculty of Arts and Sciences, University of Balamand, Kalhat, Tripoli P.O. Box 100, Lebanon.
University of Balamand · LBAmerican University of Beirut · LB

Funding

National Council for Scientific Research 1849-18
6 · The paper itself

Abstract

Cardiovascular disease as a result of atherosclerosis is a leading cause of death worldwide. Atherosclerosis is primarily caused by the dysfunction of vascular endothelial cells and the subendothelial accumulation of oxidized forms of low-density lipoprotein (LDL). Early observations have linked oxidized LDL effects in atherogenesis to the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) scavenger receptor. It was shown that LOX-1 is upregulated by many inflammatory mediators and proatherogenic stimuli including cytokines, reactive oxygen species (ROS), hemodynamic blood flow, high blood sugar levels and, most importantly, modified forms of LDL. Oxidized LDL signaling pathways in atherosclerosis were first explored using LDL that is oxidized by copper (Cuox-LDL). In our study, we used a more physiologically relevant model of LDL oxidation and showed, for the first time, that myeloperoxidase oxidized LDL (Mox-LDL) may affect human aortic endothelial cell (HAEC) function through the LOX-1 scavenger receptor. We report that Mox-LDL increases the expression of its own LOX-1 receptor in HAECs, enhancing inflammation and simultaneously decreasing tubulogenesis in the cells. We hypothesize that Mox-LDL drives endothelial dysfunction (ED) through LOX-1 which provides an initial hint to the pathways that are initiated by Mox-LDL during ED and the progression of atherosclerosis.

Indexed as

AtherosclerosisEndothelial CellsHumansLipoproteins, LDLPeroxidaseReceptors, LDLScavenger Receptors, Class ELipoproteins, LDLoxidized low density lipoproteinPeroxidaseReceptors, LDLScavenger Receptors, Class Eatherosclerosisendothelial dysfunctioninflammationLOX-1Mox-LDLtubulogenesis

Identifiers

PMID35269979
PMCPMC8910860
OpenAlexW4221016006

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.