Evidence map›Paper›PMID 26197235›Full record

ArticlePloS one2015

Foam Cell Formation In Vivo Converts Macrophages to a Pro-Fibrotic Phenotype.

Anita C Thomas, Wouter J Eijgelaar, Mat J A P Daemen, Andrew C Newby

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  6. Review
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  14. Metabolic Dysregulation in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2020
    Review
  15. Review
  16. Article
  17. Regulation of Macrophage Foam Cell Formation During Nitrogen Mustard (NM)-Induced Pulmonary Fibrosis by Lung Lipids.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  18. Alveolar Macrophage ABCG1 Deficiency Promotes Pulmonary Granulomatous Inflammation.American journal of respiratory cell and molecular biology · 2019
    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

4 authors at 4 institutions in 2 countries.

Anita C ThomasBristol Heart Institute, University of Bristol, Bristol, United Kingdom.
Wouter J EijgelaarCardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands.
Mat J A P DaemenCardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands; Academisch Medisch Centrum (AMC), Amsterdam, The Netherlands.
Andrew C NewbyBristol Heart Institute, University of Bristol, Bristol, United Kingdom.
Academic Medical Center · NLMaastricht University · NLNIHR Bristol Cardiovascular Biomedical Research Unit · GBUniversity of Bristol · GB

Funding

British Heart Foundation RG/09/006/27918
6 · The paper itself

Abstract

Formation of foam cell macrophages, which sequester extracellular modified lipids, is a key event in atherosclerosis. How lipid loading affects macrophage phenotype is controversial, with evidence suggesting either pro- or anti-inflammatory consequences. To investigate this further, we compared the transcriptomes of foamy and non-foamy macrophages that accumulate in the subcutaneous granulomas of fed-fat ApoE null mice and normal chow fed wild-type mice in vivo. Consistent with previous studies, LXR/RXR pathway genes were significantly over-represented among the genes up-regulated in foam cell macrophages. Unexpectedly, the hepatic fibrosis pathway, associated with platelet derived growth factor and transforming growth factor-β action, was also over-represented. Several collagen polypeptides and proteoglycan core proteins as well as connective tissue growth factor and fibrosis-related FOS and JUN transcription factors were up-regulated in foam cell macrophages. Increased expression of several of these genes was confirmed at the protein level in foam cell macrophages from subcutaneous granulomas and in atherosclerotic plaques. Moreover, phosphorylation and nuclear translocation of SMAD2, which is downstream of several transforming growth factor-β family members, was also detected in foam cell macrophages. We conclude that foam cell formation in vivo leads to a pro-fibrotic macrophage phenotype, which could contribute to plaque stability, especially in early lesions that have few vascular smooth muscle cells.

Indexed as

Signal TransductionAnimalsApolipoproteins EAtherosclerosisFoam CellsGene Expression ProfilingGene Expression RegulationGranulomaMaleMiceRetinoid X ReceptorsSkin DiseasesApolipoproteins ERetinoid X Receptors

Identifiers

PMID26197235
PMCPMC4510387
OpenAlexW1616573322

What OpenQuestion holds

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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.