Evidence map›Paper›PMID 33514719›Full record

ArticleNature communications2021

Single cell sequencing reveals endothelial plasticity with transient mesenchymal activation after myocardial infarction.

Lukas S Tombor, David John, Simone F Glaser, Guillermo Luxán, Elvira Forte, Milena Furtado, Nadia Rosenthal, Nina Baumgarten, Marcel H Schulz, Janina Wittig and 14 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
205citing papers in PubMed, 2 pooled it
17.4field-weighted citation impact, top 1% 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

205 citing papers in PubMed, 2 syntheses or guidelines pooled it, 289 citations in OpenAlex.

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  11. Genetics-Informed Mapping Identifies a CRIM1-Associated Endocardial Inflammatory Remodeling State in Acute Myocardial Infarction.Medical science monitor : international medical journal of experimental and clinical research · 2026
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145 more citing papers are in PubMed but not listed here.

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

24 authors at 6 institutions in 4 countries.

Lukas S TomborInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.ORCID 0000-0002-5867-576X
David JohnInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Simone F GlaserInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Guillermo LuxánInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.ORCID 0000-0001-8350-8659
Elvira ForteThe Jackson Laboratory, Bar Harbor, ME, USA.ORCID 0000-0002-5555-9122
Milena FurtadoThe Jackson Laboratory, Bar Harbor, ME, USA.
Nadia RosenthalThe Jackson Laboratory, Bar Harbor, ME, USA.
Nina BaumgartenInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.ORCID 0000-0002-5423-8634
Marcel H SchulzInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Janina WittigInstitute for Vascular Signaling, Goethe University Frankfurt, Frankfurt am Main, Germany.
Eva-Maria RoggInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Yosif ManavskiInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Ariane FischerInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Marion Muhly-ReinholzInstitute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Kathrin KleeGerman Center of Cardiovascular Research (DZHK), Frankfurt am Main, Germany.ORCID 0000-0003-2408-1282
Mario LoosoCardiopulmonary Institute, Frankfurt am Main, Germany.ORCID 0000-0003-1495-9530
Carmen SelignowDepartment of Pathology, University Giessen, Giessen, Germany.
Till AckerCardiopulmonary Institute, Frankfurt am Main, Germany.
Sofia-Iris BibliInstitute for Vascular Signaling, Goethe University Frankfurt, Frankfurt am Main, Germany.
Ingrid FlemingCardiopulmonary Institute, Frankfurt am Main, Germany.
Ralph PatrickDivision of Molecular Cardiology and Biophysics, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.ORCID 0000-0003-0956-1026
Richard P HarveyDivision of Molecular Cardiology and Biophysics, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
Wesley T Abplanalp *Institute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany.
Stefanie Dimmeler *Institute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt am Main, Germany. dimmeler@em.uni-frankfurt.de.ORCID 0000-0002-1045-2436
Goethe University Frankfurt · DEJackson Laboratory · USGiessen School of Theology · DEVictor Chang Cardiac Research Institute · AUGerman Centre for Cardiovascular Research · DEMax Planck Institute for Heart and Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells play a critical role in the adaptation of tissues to injury. Tissue ischemia induced by infarction leads to profound changes in endothelial cell functions and can induce transition to a mesenchymal state. Here we explore the kinetics and individual cellular responses of endothelial cells after myocardial infarction by using single cell RNA sequencing. This study demonstrates a time dependent switch in endothelial cell proliferation and inflammation associated with transient changes in metabolic gene signatures. Trajectory analysis reveals that the majority of endothelial cells 3 to 7 days after myocardial infarction acquire a transient state, characterized by mesenchymal gene expression, which returns to baseline 14 days after injury. Lineage tracing, using the Cdh5-CreERT2;mT/mG mice followed by single cell RNA sequencing, confirms the transient mesenchymal transition and reveals additional hypoxic and inflammatory signatures of endothelial cells during early and late states after injury. These data suggest that endothelial cells undergo a transient mes-enchymal activation concomitant with a metabolic adaptation within the first days after myocardial infarction but do not acquire a long-term mesenchymal fate. This mesenchymal activation may facilitate endothelial cell migration and clonal expansion to regenerate the vascular network.

Indexed as

AnimalsCell MovementCell PlasticityCell ProliferationCells, CulturedDisease Models, AnimalEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionGenes, ReporterHumansHuman Umbilical Vein Endothelial CellsLuminescent ProteinsMaleMiceMice, TransgenicLuminescent Proteins

Identifiers

PMID33514719
PMCPMC7846794
OpenAlexW3125573011

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.