Evidence map›Paper›PMID 29525783›Full record

ArticleJournal of the American Heart Association2018

Lipopolysaccharide Lowers Cholesteryl Ester Transfer Protein by Activating F4/80

Sam J L van der Tuin, Zhuang Li, Jimmy F P Berbée, Inge Verkouter, Linda E Ringnalda, Annette E Neele, Jan B van Klinken, Sander S Rensen, Jingyuan Fu, Menno P J de Winther and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 81 citations in OpenAlex.

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  8. Impact of High-Density Lipoproteins on Sepsis.International journal of molecular sciences · 2022
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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

14 authors at 6 institutions in 2 countries.

Sam J L van der TuinDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Zhuang LiDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Jimmy F P BerbéeDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Inge VerkouterDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Linda E RingnaldaDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Annette E NeeleDepartment of Medical Biochemistry, Academic Medical Center, Amsterdam, The Netherlands.
Jan B van KlinkenDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Sander S RensenDepartment of Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.
Jingyuan FuDepartment of Pediatrics, University of Groningen, The Netherlands.
Menno P J de WintherDepartment of Medical Biochemistry, Academic Medical Center, Amsterdam, The Netherlands.
Albert K GroenAmsterdam Diabetes Center, Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, The Netherlands.
Patrick C N RensenDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Ko Willems van DijkDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Yanan WangDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands y.wang@lumc.nl.
Leiden University Medical Center · NLAcademic Medical Center · NLLudwig-Maximilians-Universität München · DEMaastricht University · NLUniversity Medical Center Groningen · NLUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipopolysaccharide (LPS) decreases hepatic CETP (cholesteryl ester transfer protein) expression albeit that the underlying mechanism is disputed. We recently showed that plasma CETP is mainly derived from Kupffer cells (KCs). In this study, we investigated the role of KC subsets in the mechanism by which LPS reduces CETP expression. METHODS AND

resultsIn CETP-transgenic mice, LPS markedly decreased hepatic

conclusionsHepatic expression of CETP is exclusively confined to the resting KC subset (ie, F4/80

Indexed as

AnimalsAntigens, LyCalcium-Binding ProteinsCells, CulturedCholesterol Ester Transfer ProteinsDisease Models, AnimalDyslipidemiasFemaleHumansKupffer CellsLectins, C-TypeLipidsLipopolysaccharidesLiverMacrophage ActivationMaleAdgre1 protein, mouseAntigens, LyCalcium-Binding ProteinsCETP protein, humanCholesterol Ester Transfer ProteinsCLEC4F protein, mouseLectins, C-TypeLipidsLipopolysaccharidesLy-6C antigen, mouseReceptors, ComplementReceptors, G-Protein-CoupledVSIG4 protein, mouseinflammationlipids and lipoprotein metabolismlivermacrophagemarker

Identifiers

PMID29525783
PMCPMC5907564
OpenAlexW2793835122

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.