Evidence map›Paper›PMID 41313428›Full record

ArticleTissue engineering and regenerative medicine2026

Macrophage Paracrine Signalling Differentially Affects Fibroblast-Induced Collagenous Tissue Remodelling.

Hannah F M Brouwer, Amal K Mansoor, Sylvia Dekker, Carlijn V C Bouten, Keita Ito, Jasper Foolen, Anthal I P M Smits

Abstract read
In one paragraph

Article in Tissue engineering and regenerative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026
    Review
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.

Hannah F M Brouwer *Department of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.
Amal K Mansoor *Department of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.
Sylvia DekkerDepartment of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.
Carlijn V C BoutenDepartment of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.
Keita ItoDepartment of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.
Jasper FoolenDepartment of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands. JFoolen@tue.nl.
Anthal I P M SmitsDepartment of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands. a.i.p.m.smits@tue.nl.ORCID http://orcid.org/0000-0002-3665-7106

Funding

H2020 European Research Council 101042538Nederlandse Organisatie voor Wetenschappelijk Onderzoek 024.003.013
6 · The paper itself

Abstract

backgroundUpon injury, tissue repair often leads to a loss in functionality, organisation, and structure. The immune system, particularly macrophages, is crucial during tissue healing. Macrophages polarise into pro-inflammatory M1 and anti-inflammatory M2 subsets, regulating various stages of tissue healing. Macrophages steer fibroblasts in the process of extracellular matrix degradation, synthesis, and rearrangement. However, the direct role of paracrine signalling by different macrophage phenotypes on fibroblast-induced structural tissue remodelling remains elusive. Therefore, this study aimed to explore how paracrine factors from M1, M2a, and M2c macrophages affect fibroblast remodelling abilities in an in vitro model system.

methodsMacrophages were polarised in vitro, and their conditioned medium or cytokine-enriched medium containing specific macrophage-secreted factors was added to fibroblast-populated reconstituted collagen tissues.

resultsMacrophage-conditioned media led to changes in fibroblast-induced tissue compaction for all macrophage subsets. The presence of macrophage polarising factors in the conditioned medium, particularly LPS/IFNγ, and high serum levels directly affected tissue compaction and matrix remodelling gene expression. Without these confounding factors, M1 cytokine-enriched medium led to reduced tissue compaction when compared to M2a/M2c cytokine-enriched media. MMP activity analysis showed that matrix degradation likely contributed to tissue compaction.

conclusionFactors secreted by M1 macrophages resulted in reduced tissue compaction compared to M2a/M2c macrophages in an in vitro model of tissue remodelling, suggesting a diminished capacity for fibroblasts to remodel the extracellular matrix. Importantly, factors to polarize macrophages and serum are regarded as confounding factors in studying the effect of paracrine signalling by macrophages on tissue remodelling.

Indexed as

CollagenFibroblastsMacrophagesParacrine CommunicationAnimalsCulture Media, ConditionedCytokinesExtracellular MatrixHumansMiceCollagenCulture Media, ConditionedCytokinesCollagen remodellingMacrophage polarisationTissue engineering

Identifiers

PMID41313428
PMCPMC12775218

What Socratic 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 Socratic graph.