Evidence map›Paper›PMID 30451828›Full record

ArticleNature communications2018

Single cell RNA-seq and ATAC-seq analysis of cardiac progenitor cell transition states and lineage settlement.

Guangshuai Jia, Jens Preussner, Xi Chen, Stefan Guenther, Xuejun Yuan, Michail Yekelchyk, Carsten Kuenne, Mario Looso, Yonggang Zhou, Sarah Teichmann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
11.0field-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

148 citing papers in PubMed, 224 citations in OpenAlex.

  1. Review
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  4. Article
  5. Role of CHD chromatin remodelers in heart development.World journal of pediatrics : WJP · 2026
    Review
  6. Article
  7. Review
  8. Enhancer Dynamics for Gene Regulation in the Cardiovascular System.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
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  19. Article
  20. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review

88 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

11 authors at 3 institutions in 2 countries.

Guangshuai Jia *Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Jens Preussner *Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Xi Chen *Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Stefan GuentherDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Xuejun YuanDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Michail YekelchykDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Carsten KuenneDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Mario LoosoDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Yonggang ZhouDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Sarah TeichmannWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.ORCID http://orcid.org/0000-0002-6294-6366
Thomas BraunDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany. thomas.braun@mpi-bn.mpg.de.
Max Planck Institute for Heart and Lung Research · DEEuropean Bioinformatics Institute · GBWellcome Sanger Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Formation and segregation of cell lineages forming the heart have been studied extensively but the underlying gene regulatory networks and epigenetic changes driving cell fate transitions during early cardiogenesis are still only partially understood. Here, we comprehensively characterize mouse cardiac progenitor cells (CPCs) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing and transposase-accessible chromatin profiling (ATAC-seq). By leveraging on cell-to-cell transcriptome and chromatin accessibility heterogeneity, we identify different previously unknown cardiac subpopulations. Reconstruction of developmental trajectories reveal that multipotent Isl1

Indexed as

Gene Expression Regulation, DevelopmentalTranscriptomeAnimalsBody PatterningCell DifferentiationCell LineageChromatinEmbryo, MammalianGene Regulatory NetworksHomeobox Protein Nkx-2.5LIM-Homeodomain ProteinsMiceMice, Inbred C57BLMice, TransgenicMouse Embryonic Stem CellsMyocytes, CardiacChromatinHomeobox Protein Nkx-2.5insulin gene enhancer binding protein Isl-1LIM-Homeodomain ProteinsNkx2-5 protein, mouseTranscription Factors

Identifiers

PMID30451828
PMCPMC6242939
OpenAlexW2901006884

What OpenQuestion holds

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LicenceCC BY
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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.