Evidence map›Paper›PMID 31162546›Full record

ArticleEuropean heart journal2019

Single-cell transcriptome analyses reveal novel targets modulating cardiac neovascularization by resident endothelial cells following myocardial infarction.

Ziwen Li, Emmanouil G Solomonidis, Marco Meloni, Richard S Taylor, Rodger Duffin, Ross Dobie, Marlene S Magalhaes, Beth E P Henderson, Pieter A Louwe, Gabriela D'Amico and 8 more

Abstract read
In one paragraph

Article in European heart journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

142 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. CD157Stem cell reports · 2026
    Article
  5. Aging and DNA damage are associated with the development of endothelial cell clonal expansion.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Dissecting endothelial cell heterogeneity with new tools.Cell regeneration (London, England) · 2025
    Review
  17. Cardiovascular Disease and Cancer: A Dangerous Liaison.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  18. Article
  19. Review
  20. Article

82 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Ziwen LiCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Emmanouil G SolomonidisCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Marco MeloniCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Richard S TaylorCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Rodger DuffinCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Ross DobieCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Marlene S MagalhaesCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Beth E P HendersonCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Pieter A LouweCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Gabriela D'AmicoCentre for Tumour Biology, Barts Cancer Institute, CRUK-Barts Centre, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, UK.
Kairbaan M Hodivala-DilkeCentre for Tumour Biology, Barts Cancer Institute, CRUK-Barts Centre, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, UK.
Ajay M ShahDepartment for Cardiovascular Sciences, King's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.
Nicholas L MillsCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Benjamin D SimonsCavendish Laboratory, Department of Physics, University of Cambridge, J.J. Thomson Avenue, Cambridge, UK.
Gillian A GrayCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Neil C HendersonCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Andrew H BakerCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Mairi BrittanCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.

Funding

British Heart Foundation CH/11/2/28733British Heart Foundation FS/10/024/28266British Heart Foundation FS/16/14/32023British Heart Foundation FS/16/4/31831British Heart Foundation RG/14/3/30706British Heart Foundation RM/17/3/33381Cancer Research UK 12007Cancer Research UK 18673Medical Research Council MC_PC_12009Wellcome Trust
6 · The paper itself

Abstract

aimsA better understanding of the pathways that regulate regeneration of the coronary vasculature is of fundamental importance for the advancement of strategies to treat patients with heart disease. Here, we aimed to investigate the origin and clonal dynamics of endothelial cells (ECs) associated with neovascularization in the adult mouse heart following myocardial infarction (MI). Furthermore, we sought to define murine cardiac endothelial heterogeneity and to characterize the transcriptional profiles of pro-angiogenic resident ECs in the adult mouse heart, at single-cell resolution. METHODS AND

resultsAn EC-specific multispectral lineage-tracing mouse (Pdgfb-iCreERT2-R26R-Brainbow2.1) was used to demonstrate that structural integrity of adult cardiac endothelium following MI was maintained through clonal proliferation by resident ECs in the infarct border region, without significant contributions from bone marrow cells or endothelial-to-mesenchymal transition. Ten transcriptionally discrete heterogeneous EC states, as well as the pathways through which each endothelial state is likely to enhance neovasculogenesis and tissue regeneration following ischaemic injury were defined. Plasmalemma vesicle-associated protein (Plvap) was selected for further study, which showed an endothelial-specific and increased expression in both the ischaemic mouse and human heart, and played a direct role in regulating human endothelial proliferation in vitro.

conclusionWe present a single-cell gene expression atlas of cardiac specific resident ECs, and the transcriptional hierarchy underpinning endogenous vascular repair following MI. These data provide a rich resource that could assist in the development of new therapeutic interventions to augment endogenous myocardial perfusion and enhance regeneration in the injured heart.

Indexed as

AnimalsCell ProliferationEndothelial CellsGene Expression ProfilingHumansMiceMice, TransgenicMyocardial InfarctionMyocardiumNeovascularization, PhysiologicSingle-Cell AnalysisTranscriptomeCell proliferationEndothelial cellsLineage tracingMyocardial infarctionSingle-cell RNA sequencingTherapeutic angiogenesis

Identifiers

PMID31162546
PMCPMC6685329

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Registered trials

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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.