Evidence map›Paper›PMID 35327330›Full record

ArticleBiomedicines2022

Fibrin, Bone Marrow Cells and Macrophages Interactively Modulate Cardiomyoblast Fate.

Inês Borrego, Aurélien Frobert, Guillaume Ajalbert, Jérémy Valentin, Cyrielle Kaltenrieder, Benoît Fellay, Michael Stumpe, Stéphane Cook, Joern Dengjel, Marie-Noëlle Giraud

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Distinct Hemostasis and Blood Composition in Spiny MouseInternational journal of molecular sciences · 2024
    Article
  4. Review
  5. Article
  6. 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

10 authors at 2 institutions in 1 country.

Inês BorregoDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
Aurélien FrobertDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
Guillaume AjalbertDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.ORCID 0000-0003-4637-2232
Jérémy ValentinDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
Cyrielle KaltenriederDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
Benoît FellayHFR Hôpital Fribourgeois, 1708 Fribourg, Switzerland.ORCID 0000-0001-5270-629X
Michael StumpeDepartment of Biology, University of Fribourg, 1700 Fribourg, Switzerland.
Stéphane CookDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
Joern DengjelDepartment of Biology, University of Fribourg, 1700 Fribourg, Switzerland.ORCID 0000-0002-9453-4614
Marie-Noëlle GiraudDepartment of EMC, Faculty of Sciences and Medicine, University of Fribourg, 1700 Fribourg, Switzerland.ORCID 0000-0003-3228-6827
University of Fribourg · CHRéseau Fribourgeois de Santé Mentale · CH

Funding

Swiss National Science Foundation 310030_149986
6 · The paper itself

Abstract

Interactions between macrophages, cardiac cells and the extracellular matrix are crucial for cardiac repair following myocardial infarction (MI). We hypothesized that cell-based treatments might modulate these interactions. After validating that bone marrow cells (BMC) associated with fibrin lowered the infarct extent and improved cardiac function, we interrogated the influence of fibrin, as a biologically active scaffold, on the secretome of BMC and the impact of their association on macrophage fate and cardiomyoblast proliferation. In vitro, BMC were primed with fibrin (F-BMC). RT-PCR and proteomic analyses showed that fibrin profoundly influenced the gene expression and the secretome of BMCs. Consequently, the secretome of F-BMC increased the spreading of cardiomyoblasts and showed an alleviated immunomodulatory capacity. Indeed, the proliferation of anti-inflammatory macrophages was augmented, and the phenotype of pro-inflammatory switched as shown by downregulated

Indexed as

cell communicationcell primingfibrininflammationmacrophagessecretome

Identifiers

PMID35327330
PMCPMC8945703
OpenAlexW4226063223

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.