Evidence map›Paper›PMID 25124749›Full record

ArticleJournal of cellular and molecular medicine2014

Complement factor C5a induces atherosclerotic plaque disruptions.

Anouk Wezel, Margreet R de Vries, H Maxime Lagraauw, Amanda C Foks, Johan Kuiper, Paul H A Quax, Ilze Bot

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Exploring the intersection of atherosclerosis and Alzheimer's disease: the role of inflammation and complement activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  5. Review
  6. Article
  7. Role of C-Reactive Protein, An Inflammatory Biomarker in The Development of Atherosclerosis and Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Frontiers in immunology · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Alternative C3 Complement System: Lipids and Atherosclerosis.International journal of molecular sciences · 2021
    Article
  17. The Role of Immunomodulation in Vein Graft Remodeling and Failure.Journal of cardiovascular translational research · 2021
    Review
  18. 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

7 authors at 3 institutions in 1 country.

Anouk WezelDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands; Department of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
Margreet R de Vries
H Maxime Lagraauw
Amanda C Foks
Johan Kuiper
Paul H A Quax
Ilze Bot
Centre for Human Drug Research · NLLeiden University · NLLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement factor C5a and its receptor C5aR are expressed in vulnerable atherosclerotic plaques; however, a causal relation between C5a and plaque rupture has not been established yet. Accelerated atherosclerosis was induced by placing vein grafts in male apoE(-/-) mice. After 24 days, when advanced plaques had developed, C5a or PBS was applied locally at the lesion site in a pluronic gel. Three days later mice were killed to examine the acute effect of C5a on late stage atherosclerosis. A significant increase in C5aR in the plaque was detectable in mice treated with C5a. Lesion size and plaque morphology did not differ between treatment groups, but interestingly, local treatment with C5a resulted in a striking increase in the amount of plaque disruptions with concomitant intraplaque haemorrhage. To identify the potential underlying mechanisms, smooth muscle cells and endothelial cells were treated in vitro with C5a. Both cell types revealed a marked increase in apoptosis after stimulation with C5a, which may contribute to lesion instability in vivo. Indeed, apoptosis within the plaque was seen to be significantly increased after C5a treatment. We here demonstrate a causal role for C5a in atherosclerotic plaque disruptions, probably by inducing apoptosis. Therefore, intervention in complement factor C5a signalling may be a promising target in the prevention of acute atherosclerotic complications.

Indexed as

ApoptosisAnimalsApolipoproteins ECells, CulturedComplement C5aEndothelium, VascularImmunoenzyme TechniquesMaleMiceMice, KnockoutMyocytes, Smooth MusclePlaque, AtheroscleroticReal-Time Polymerase Chain ReactionReceptor, Anaphylatoxin C5aReverse Transcriptase Polymerase Chain ReactionRNA, MessengerApolipoproteins EComplement C5aReceptor, Anaphylatoxin C5aRNA, MessengerapoptosisatherosclerosisC5aplaque rupture

Identifiers

PMID25124749
PMCPMC4244017
OpenAlexW2045800862

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.