Evidence map›Paper›PMID 29467221›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2018

Vascular Development.

Mark W Majesky

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.5field-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

52 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Embryology of the Vascular System: Implications for Variants.Seminars in interventional radiology · 2025
    Review
  17. Review
  18. The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025
    Review
  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

1 author at 1 institution in 1 country.

Mark W MajeskyFrom the Center for Developmental Biology and Regenerative Medicine, Seattle Children's Research Institute, WA; and Departments of Pediatrics and Pathology, University of Washington, Seattle. mwm84@uw.edu.
University of Washington · US

Funding

Reprogramming of mature smooth muscle cells to vascular progenitor cellsR01HL121877 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MARK W. MAJESKY, Mary CM Weiser-Evans · 2015 to 2026
$7.8M
Adventitial-medial interactions in thoracic aortic diseasesR01HL133723 · NHLBI · UNIVERSITY OF KENTUCKY · PI DAUGHERTY, ALAN · 2016 to 2019
$2.9M
Resident Progenitor Cells in the AdventitiaR01HL123650 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI MAJESKY, MARK W. · 2014 to 2017
$2.4M
NHLBI NIH HHS R01 HL121877NHLBI NIH HHS R01 HL123650NHLBI NIH HHS R01 HL133723
6 · The paper itself

Abstract

The vascular system forms as a branching network of endothelial cells that acquire identity as arterial, venous, hemogenic, or lymphatic. Endothelial specification depends on gene targets transcribed by Ets domain-containing factors, including Ets variant gene 2 (Etv2), together with the activity of chromatin-remodeling complexes containing Brahma-related gene-1 (Brg1). Once specified and assembled into vessels, mechanisms regulating lumen diameter and axial growth ensure that the structure of the branching vascular network matches the need for perfusion of target tissues. In addition, blood vessels provide important morphogenic cues that guide or direct the development of organs forming around them. As the embryo grows and lumen diameters increase, smooth muscle cells wrap around the nascent vessel walls to provide mechanical strength and vasomotor control of the circulation. Increasing mechanical stretch and wall strain promote smooth muscle cell differentiation via coupling of actin cytoskeletal remodeling to myocardin and serum response factor-dependent transcription. Remodeling of artery walls by developmental signaling pathways reappears in postnatal blood vessels during physiological and pathological adaptation to vessel wall injury, inflammation, or chronic hypoxia. Recent reports providing insights into major steps in vascular development are reviewed here with a particular emphasis on studies that have been recently published in

Indexed as

Cell DifferentiationCell LineageNeovascularization, PhysiologicAnimalsArteriesCell CommunicationEndothelial CellsGene Expression Regulation, DevelopmentalHumansMyocytes, Smooth MusclePhenotypeSignal Transductionadventitiacell lineageendothelial cellsinflammationmyocardin

Identifiers

PMID29467221
PMCPMC5927597
OpenAlexW4236713287

What OpenQuestion holds

Textmetadata
LicenceTDM
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.