Evidence map›Paper›PMID 37001515›Full record

ArticleStem cell reports2023

Epicardially secreted fibronectin drives cardiomyocyte maturation in 3D-engineered heart tissues.

Lay Ping Ong, Johannes Bargehr, Vincent R Knight-Schrijver, Jonathan Lee, Maria Colzani, Semih Bayraktar, William G Bernard, Silvia Marchiano, Alessandro Bertero, Charles E Murry and 2 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  7. Cell-Instructive Biomaterials with Native-Like Biochemical Complexity.Annual review of biomedical engineering · 2025
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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 3 institutions in 3 countries.

Lay Ping OngWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK. Electronic address: lpo20@cam.ac.uk.
Johannes BargehrWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
Vincent R Knight-SchrijverWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
Jonathan LeeWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
Maria ColzaniWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
Semih BayraktarWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
William G BernardWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
Silvia MarchianoDepartments of Laboratory Medicine & Pathology, Bioengineering, and Medicine/Cardiology, University of Washington, Seattle, WA, USA; Center for Cardiovascular Biology, Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA, USA.
Alessandro BerteroMolecular Biotechnology Center, Department of Molecular Biotechnology and Health Sciences, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Charles E MurryDepartments of Laboratory Medicine & Pathology, Bioengineering, and Medicine/Cardiology, University of Washington, Seattle, WA, USA; Center for Cardiovascular Biology, Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA, USA.
Laure GambardellaWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK.
Sanjay SinhaWellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK; Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, ACCI Level 6, Hills Road, Box 110, Cambridge CB2 0QQ, UK. Electronic address: ss661@cam.ac.uk.
Wellcome/MRC Cambridge Stem Cell Institute · GBUniversity of Washington · USUniversity of Turin · IT

Funding

British Heart Foundation FS/18/46/33663British Heart Foundation RM/13/3/30159British Heart Foundation RM/17/2/33380British Heart Foundation SP/15/7/31561Medical Research Council MC_PC_17230Wellcome TrustWellcome Trust 203151/Z/16/ZWellcome Trust 203568/Z/16/Z
6 · The paper itself

Abstract

Ischemic heart failure is due to irreversible loss of cardiomyocytes. Preclinical studies showed that human pluripotent stem cell (hPSC)-derived cardiomyocytes could remuscularize infarcted hearts and improve cardiac function. However, these cardiomyocytes remained immature. Incorporating hPSC-derived epicardial cells has been shown to improve cardiomyocyte maturation, but the exact mechanisms are unknown. We posited epicardial fibronectin (FN1) as a mediator of epicardial-cardiomyocyte crosstalk and assessed its role in driving hPSC-derived cardiomyocyte maturation in 3D-engineered heart tissues (3D-EHTs). We found that the loss of FN1 with peptide inhibition F(pUR4), CRISPR-Cas9-mediated FN1 knockout, or tetracycline-inducible FN1 knockdown in 3D-EHTs resulted in immature cardiomyocytes with decreased contractile function, and inefficient Ca

Indexed as

Induced Pluripotent Stem CellsPluripotent Stem CellsCell DifferentiationFibronectinsHumansMyocytes, CardiacFibronectinscardiomyocytesengineered heart tissuesepicardiumfibronectinmaturation

Identifiers

PMID37001515
PMCPMC10147941
OpenAlexW4361269669

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.