Evidence map›Paper›PMID 30948775›Full record

ArticleScientific reports2019

Serum of patients with acute myocardial infarction prevents inflammation in iPSC-cardiomyocytes.

Katherine Sattler, Ibrahim El-Battrawy, Zhihan Zhao, Christoph Schrottenberg, Gökhan Yücel, Huan Lan, Xin Li, Siegfried Lang, Wolfram-Hubertus Zimmermann, Lukas Cyganek and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Infarct Zone: a Novel Platform for Exosome Trade in Cardiac Tissue Regeneration.Journal of cardiovascular translational research · 2020
    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

17 authors at 5 institutions in 2 countries.

Katherine SattlerFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Ibrahim El-BattrawyFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany. Ibrahim.El-Battrawy@umm.de.
Zhihan ZhaoFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Christoph SchrottenbergFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Gökhan YücelFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Huan LanFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Xin LiFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Siegfried LangFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Wolfram-Hubertus ZimmermannDZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim and Göttingen, Göttingen, Germany.
Lukas CyganekDZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim and Göttingen, Göttingen, Germany.
Jochen UtikalSkin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg and Department of Dermatology, Venereology and Allergology, University Medical Center Mannheim, University of Heidelberg, Mannheim, Germany.ORCID http://orcid.org/0000-0001-5316-0241
Thomas WielandDZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim and Göttingen, Göttingen, Germany.ORCID http://orcid.org/0000-0001-8262-8261
Ursula RavensInstitue of Experimental Cardiovascular Medicine, University Heart Centre Freiburg, Bad Krozingen, Freiburg, Germany.
Karen BiebackInstitute for Transfusion Medicine and Immunology, Mannheim, Germany.
Martin BorggrefeFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Xiaobo ZhouFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Ibrahim AkinFirst Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Heidelberg University · DEGerman Cancer Research Center · DEGerman Centre for Cardiovascular Research · DEUniversitäts-Herzzentrum Freiburg-Bad Krozingen · DEUniversitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myocardial infarction (MI) evokes a systemic inflammatory response and locally the degradation of the necrotic tissue, followed by scar formation. The mechanisms for containment of the infarct zone are not studied well. The study aimed to examine the response of healthy cardiomyocytes to serum of patients with myocardial infarction. Human iPSC-cardiomyocytes (iPSC-CM) generated from two healthy donors were incubated with serum of patients with MI with and without ventricular fibrillation (VF) or of healthy controls. Different cell adhesion molecules were studied by flow cytometry and immunostaining. Cellular electrophysiology was studied by patch clamp. The cell adhesion molecules CD54/ICAM-1, CD58/LFA-3 and CD321/JAM-A were expressed on iPSC-CM within the plasma membrane. Incubation with serum of MI patients reduced the levels of expression of CD54/ICAM-1 and CD321/JAM-A by 15-20%. VF serum was less effective than serum of MI patients without VF. MI serum or VF serum did not affect resting potential, action potential duration or maximum depolarization velocity. Myocardial infarction serum exerts anti-inflammatory effects on healthy cardiomyocytes without affecting their electrical activity, thus helping to contain the infarct zone and to protect healthy tissue. Ventricular fibrillation during MI drives healthy cardiomyocytes towards a pro-inflammatory phenotype.

Indexed as

AdultAgedArrhythmias, CardiacCell AdhesionCell Adhesion MoleculesFemaleHumansInduced Pluripotent Stem CellsInflammationMaleMiddle AgedMyocardial InfarctionMyocytes, CardiacTranscriptomeVentricular FibrillationCell Adhesion Molecules

Identifiers

PMID30948775
PMCPMC6449343
OpenAlexW2935252922

What OpenQuestion holds

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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.