Evidence map›Paper›PMID 27762264›Full record

ArticleNature communications2016

TREM-1 links dyslipidemia to inflammation and lipid deposition in atherosclerosis.

Daniel Zysset, Benjamin Weber, Silvia Rihs, Jennifer Brasseit, Stefan Freigang, Carsten Riether, Yara Banz, Adelheid Cerwenka, Cedric Simillion, Pedro Marques-Vidal and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
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  6. Article
  7. Article
  8. Epithelial pyroptosis-induced TREM1Cell death discovery · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Tissue-resident CCR2Cell reports · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Therapeutic delivery of CCL2 modulates immune response and restores host-microbe homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article
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

13 authors at 3 institutions in 2 countries.

Daniel ZyssetDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
Benjamin WeberDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
Silvia RihsDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
Jennifer BrasseitDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
Stefan FreigangDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.ORCID 0000-0003-4438-7828
Carsten RietherDepartment of Clinical Research, Tumor Immunology, University of Bern, CH-3008 Bern, Switzerland.ORCID 0000-0001-7512-513X
Yara BanzDivision of Clinical Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
Adelheid CerwenkaInnate Immunity Group, German Cancer Research Center, D-69120 Heidelberg, Germany.
Cedric SimillionDepartment of Clinical Research, Tumor Immunology, University of Bern, CH-3008 Bern, Switzerland.
Pedro Marques-VidalDepartment of Internal Medicine, Internal Medicine, Lausanne University Hospital, CH-1011 Lausanne, Switzerland.
Adrian F OchsenbeinDepartment of Clinical Research, Tumor Immunology, University of Bern, CH-3008 Bern, Switzerland.
Leslie SaurerDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
Christoph MuellerDivision of Experimental Pathology, Institute of Pathology, University of Bern, CH-3008 Bern, Switzerland.
University of Bern · CHGerman Cancer Research Center · DEUniversity of Lausanne · CH

Funding

Swiss National Science Foundation 152872
6 · The paper itself

Abstract

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune responses, but its significance in non-infectious diseases remains unclear. Here, we demonstrate that TREM-1 promotes cardiovascular disease by exacerbating atherosclerosis. TREM-1 is expressed in advanced human atheromas and is highly upregulated under dyslipidemic conditions on circulating and on lesion-infiltrating myeloid cells in the Apoe

Indexed as

AnimalsAntigens, LyAortaApolipoproteins EAtherosclerosisCell DifferentiationCell LineCholesterolCytokinesDiet, High-FatDisease Models, AnimalDyslipidemiasFemaleFoam CellsGene Expression RegulationHumansAntigens, LyApolipoproteins ECholesterolCytokinesLy-6C antigen, mouseTREM1 protein, humanTREM1 protein, mouseTriggering Receptor Expressed on Myeloid Cells-1

Identifiers

PMID27762264
PMCPMC5080444
OpenAlexW2537298466

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.