Evidence map›Paper›PMID 24391353›Full record

ReviewMediators of inflammation2013

Mesenchymal stem cell therapy for cardiac inflammation: immunomodulatory properties and the influence of toll-like receptors.

F van den Akker, S C A de Jager, J P G Sluijter

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.6field-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

58 citing papers in PubMed, 115 citations in OpenAlex.

  1. Review
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  11. 2D Materials for Cardiac Tissue Repair and Regeneration.Frontiers in cardiovascular medicine · 2022
    Review
  12. Regenerative medicine technologies applied to transplant medicine. An update.Frontiers in bioengineering and biotechnology · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
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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

3 authors at 3 institutions in 2 countries.

F van den AkkerDepartment of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
S C A de JagerDepartment of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
J P G SluijterDepartment of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands ; ICIN-Netherlands Heart Institute, Catharijnesingel 52, 3511 GC Utrecht, The Netherlands.
Heidelberg University · DEUniversity Hospital Heidelberg · DEUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAfter myocardial infarction (MI), the inflammatory response is indispensable for initiating reparatory processes. However, the intensity and duration of the inflammation cause additional damage to the already injured myocardium. Treatment with mesenchymal stem cells (MSC) upon MI positively affects cardiac function. This happens likely via a paracrine mechanism. As MSC are potent modulators of the immune system, this could influence this postinfarct immune response. Since MSC express toll-like receptors (TLR), danger signal (DAMP) produced after MI could influence their immunomodulatory properties. SCOPE OF REVIEW: Not much is known about the direct immunomodulatory efficiency of MSC when injected in a strong inflammatory environment. This review focuses first on the interactions between MSC and the immune system. Subsequently, an overview is provided of the effects of DAMP-associated TLR activation on MSC and their immunomodulative properties after myocardial infarction. MAJOR

conclusionsMSC can strongly influence most cell types of the immune system. TLR signaling can increase and decrease this immunomodulatory potential, depending on the available ligands. Although reports are inconsistent, TLR3 activation may boost immunomodulation by MSC, while TLR4 activation suppresses it. GENERAL SIGNIFICANCE: Elucidating the effects of TLR activation on MSC could identify new preconditioning strategies which might improve their immunomodulative properties.

Indexed as

Stem Cell TransplantationAnimalsB-LymphocytesCell DifferentiationCell MovementCell ProliferationHumansImmunomodulationInflammationLigandsMacrophagesMesenchymal Stem CellsMiceMonocytesMyocardial InfarctionMyocardiumLigandsTLR3 protein, humanTLR4 protein, humanToll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID24391353
PMCPMC3872440
OpenAlexW2090864977

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.