Evidence map›Paper›PMID 26367277›Full record

Trial reportPloS one2015

Lipocalin (LCN) 2 Mediates Pro-Atherosclerotic Processes and Is Elevated in Patients with Coronary Artery Disease.

Raghav Oberoi, Eskindir P Bogalle, Lukas A Matthes, Harald Schuett, Ann-Kathrin Koch, Karsten Grote, Bernhard Schieffer, Jutta Schuett, Maren Luchtefeld

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 40 citations in OpenAlex.

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  18. Plasma Lipocalin-2 and Adiponectin are Affected by Obesity Rather Than Type 2 Diabetes Mellitus per se.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
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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

9 authors at 2 institutions in 1 country.

Raghav OberoiDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Eskindir P BogalleDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Lukas A MatthesDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Harald SchuettDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Ann-Kathrin KochDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Karsten GroteDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Bernhard SchiefferDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Jutta SchuettDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Maren LuchtefeldDepartment of Cardiology and Angiology, Philipps-University Marburg, Marburg, Germany.
Philipps University of Marburg · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipocalin (LCN) 2 is associated with multiple acute and chronic inflammatory diseases but the underlying molecular and cellular mechanisms remain unclear. Here, we investigated whether LCN2 is released from macrophages and contributes to pro-atherosclerotic processes and whether LCN2 plasma levels are associated with the severity of coronary artery disease progression in humans. METHODS AND

resultsIn an autocrine-paracrine loop, tumor necrosis factor (TNF)-α promoted the release of LCN2 from murine bone-marrow derived macrophages (BMDM) and vice versa. Moreover, LCN2 stimulation of BMDM led to up-regulation of M1 macrophage markers. In addition, enhanced migration of monocytic J774A.1 cells towards LCN2 was observed. Furthermore, LCN2 increased the expression of the scavenger receptors Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as well as scavenger receptor class A-1 (SRA-1) and induced the conversion of macrophages to foam cells. In atherosclerotic lesions of low density lipoprotein receptor-deficient (ldlr-/-) mice fed a high fat, high cholesterol diet, LCN2 was found to be co-localized with macrophages in the shoulder region of the atherosclerotic plaque. In addition, LCN2 plasma levels were significantly increased in plasma samples of these mice. Finally, LCN2 plasma levels correlated with the severity of coronary artery disease (CAD) in patients as determined by coronary angiography.

conclusionsHere we demonstrated that LCN2 plays a pivotal role in processes involved in atherogenesis by promoting polarization and migration of monocytic cells and development of macrophages towards foam cells. Moreover, LCN2 may be used as a prognostic marker to determine the status of CAD progression.

Indexed as

Acute-Phase ProteinsAnimalsBone Marrow CellsCell LineCoronary AngiographyCoronary Artery DiseaseFemaleFoam CellsHumansLipocalin-2LipocalinsMaleMiceMice, KnockoutOncogene ProteinsProto-Oncogene ProteinsAcute-Phase ProteinsLCN2 protein, humanLcn2 protein, mouseLDLR protein, humanLipocalin-2LipocalinsMSR1 protein, humanOLR1 protein, humanOlr1 protein, mouseOncogene ProteinsProto-Oncogene ProteinsReceptors, LDLScavenger Receptors, Class AScavenger Receptors, Class E

Identifiers

PMID26367277
PMCPMC4569430
OpenAlexW2218540888

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Registered trials

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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.