Evidence map›Paper›PMID 32309541›Full record

ArticleDiscoveries (Craiova, Romania)2014

Novel insights into the mechanism of cell-based therapy after chronic myocardial infarction.

Alexander Schuh, Britta Butzbach, Adelina Curaj, Sakine Simsekyilmaz, Octavian Bucur, Isabela Kanzler, Bernd Deneke, Simone Konschalla, Andreas Kroh, Tolga Taha Sönmez and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Discoveries (Craiova, Romania), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Alexander SchuhDepartment of Cardiology and Pulmonology, Medical Faculty, RWTH Aachen University, Germany.
Britta ButzbachDepartment of Cardiology and Pulmonology, Medical Faculty, RWTH Aachen University, Germany.
Adelina CurajInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
Sakine SimsekyilmazInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
Octavian BucurDepartment of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA.
Isabela KanzlerInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
Bernd DenekeInterdisciplinary Centre for Clinical Research (IZKF) Aachen, RWTH Aachen University, Aachen, Germany.
Simone KonschallaInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
Andreas KrohInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
Tolga Taha SönmezInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
Nikolaus MarxDepartment of Cardiology and Pulmonology, Medical Faculty, RWTH Aachen University, Germany.
Elisa A LiehnInstitute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany.
RWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell transplantation therapy is considered a novel and promising strategy in regenerative medicine. Recent studies point out that paracrine effects and inflammation induced by transplanted cells are key factors for the improvement of myocardial function. The present study aims at differentiating paracrine effects from inflammatory reactions after cell transplantation. Therefore, in vitro induced apoptotic bodies were transplanted after myocardial infarction in a rat model. Eight weeks after transplantation, the functional results showed no improvement in left ventricular function. Histological analysis revealed no significant differences in the amount of infiltrated cells and collagen content did not differ among the four groups, which sustains the functional data. Surprisingly, angiogenesis increased in groups with apoptotic bodies derived from HUVEC and endothelial progenitor cells, but not from fibroblasts. A complex genetic analysis of apoptotic bodies indicated that miRNAs could be responsible for these changes. Our study demonstrates that inflammatory reaction is critical for scar remodelling and improvement of the heart function after late cell therapy, while neoangiogenesis alone is not sufficient to improve heart function.

Indexed as

apoptotic bodiescell therapymechanismsmicroRNAsmyocardial infarctiontransplantation

Identifiers

PMID32309541
PMCPMC6941593
OpenAlexW2171575578

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.