Evidence map›Paper›PMID 34497373›Full record

ArticleNature cell biology2021

Perinatal angiogenesis from pre-existing coronary vessels via DLL4-NOTCH1 signalling.

Pengfei Lu, Yidong Wang, Yang Liu, Yifeng Wang, Bingruo Wu, Deyou Zheng, Richard P Harvey, Bin Zhou

Abstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. FMO2 Promotes Angiogenesis via Regulation of N-Acetylornithine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
  6. mExperimental & molecular medicine · 2025
    Review
  7. Dissecting endothelial cell heterogeneity with new tools.Cell regeneration (London, England) · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Epicardium and Coronary Vessels.Advances in experimental medicine and biology · 2024
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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

8 authors at 3 institutions in 3 countries.

Pengfei Lu *Department of Genetics, Albert Einstein College of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-6698-276X
Yidong Wang *Cardiovascular Research Center, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Yang LiuDepartment of Genetics, Albert Einstein College of Medicine, New York, NY, USA.
Yifeng WangDepartment of Cardiology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Bingruo WuDepartment of Genetics, Albert Einstein College of Medicine, New York, NY, USA.
Deyou ZhengDepartment of Genetics, Albert Einstein College of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0003-4354-5337
Richard P HarveyDevelopmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Sydney, New South Wales, Australia.ORCID http://orcid.org/0000-0002-9950-9792
Bin ZhouDepartment of Genetics, Albert Einstein College of Medicine, New York, NY, USA. bin.zhou@einsteinmed.org.ORCID http://orcid.org/0000-0003-0832-4002
Albert Einstein College of Medicine · USJiangsu Province Hospital · CNVictor Chang Cardiac Research Institute · AU

Funding

Molecular and Cellular Mechanisms in Coronary Artery Development and AnomaliesR01HL133120 · NHLBI · UNIVERSITY OF CHICAGO · PI BIN ZHOU · 2016 to 2026
$4.6M
NHLBI NIH HHS R01 HL133120
6 · The paper itself

Abstract

New coronary vessels are added to the heart around birth to support postnatal cardiac growth. Here we show that, in late fetal development, the embryonic coronary plexus at the inner myocardium of the ventricles expresses the angiogenic signalling factors VEGFR3 and DLL4 and generates new coronary vessels in neonates. Contrary to a previous model in which the formation of new coronary vessels in neonates from ventricular endocardial cells was proposed, we find that late fetal and neonatal ventricular endocardial cells lack angiogenic potential and do not contribute to new coronary vessels. Instead, we show using lineage-tracing as well as gain- and loss-of-function experiments that the pre-existing embryonic coronary plexus at the inner myocardium undergoes angiogenic expansion through the DLL4-NOTCH1 signalling pathway to vascularize the expanding myocardium. We also show that the pre-existing coronary plexus revascularizes the regenerating neonatal heart through a similar mechanism. These findings provide a different model of neonatal coronary angiogenesis and regeneration, potentially informing cardiovascular medicine.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCalcium-Binding ProteinsCoronary VesselsEndothelial CellsEndothelium, VascularHeartHeart VentriclesMice, TransgenicMorphogenesisMyocardiumNeovascularization, PathologicNeovascularization, PhysiologicReceptor, Notch1Signal TransductionAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsDLL4 protein, mouseNotch1 protein, mouseReceptor, Notch1

Identifiers

PMID34497373
OpenAlexW3196524996

What OpenQuestion holds

Textmetadata
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.