Evidence map›Paper›PMID 21814576›Full record

ArticlePloS one2011

Myeloid IκBα deficiency promotes atherogenesis by enhancing leukocyte recruitment to the plaques.

Pieter Goossens, Monique N Vergouwe, Marion J J Gijbels, Danielle M J Curfs, Johannes H G van Woezik, Marten A Hoeksema, Sofia Xanthoulea, Pieter J M Leenen, Rudolf A Rupec, Marten H Hofker and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
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  5. Review
  6. Review
  7. Article
  8. Article
  9. The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
  10. Review
  11. Review
  12. Article
  13. IKKβ links vascular inflammation to obesity and atherosclerosis.The Journal of experimental medicine · 2014
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. NF-κB signaling in inflammation.Signal transduction and targeted therapy
    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

11 authors at 4 institutions in 2 countries.

Pieter GoossensDepartment of Molecular Genetics, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Monique N Vergouwe
Marion J J Gijbels
Danielle M J Curfs
Johannes H G van Woezik
Marten A Hoeksema
Sofia Xanthoulea
Pieter J M Leenen
Rudolf A Rupec
Marten H Hofker
Menno P J de Winther
Maastricht University · NLErasmus MC · NLLudwig-Maximilians-Universität München · DEUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the transcription factor NF-κB appears to be involved in different stages of atherogenesis. In this paper we investigate the role of NF-κB inhibitor IκBα in atherosclerosis. Myeloid-specific deletion of IκBα results in larger and more advanced lesions in LDL-R-deficient mice without affecting the compositional phenotype of the plaques or systemic inflammatory markers in the plasma. We show that IκBα-deleted macrophages display enhanced adhesion to an in vitro endothelial cell layer, coinciding with an increased expression of the chemokine CCL5. Also, in vivo we found that IκBα(del) mice had more leukocytes adhering to the luminal side of the endothelial cell layers that cover the atherosclerotic plaques. Moreover, we introduce ER-MP58 in this paper as a new immunohistochemical tool for quantifying newly recruited myeloid cells in the atherosclerotic lesion. This staining confirms that in IκBα(del) mice more leukocytes are attracted to the plaques. In conclusion, we show that IκBα deletion in myeloid cells promotes atherogenesis, probably through an induced leukocyte recruitment to plaques.

Indexed as

AnimalsApolipoproteins EAtherosclerosisBlotting, WesternBone Marrow TransplantationCell AdhesionEndothelium, VascularFemaleI-kappa B ProteinsImmunoenzyme TechniquesInflammationLeukocytesMacrophagesMiceMice, Inbred C57BLMice, KnockoutApolipoproteins EI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mouseReceptors, LDL

Identifiers

PMID21814576
PMCPMC3141029
OpenAlexW2134433534

What OpenQuestion holds

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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.