Evidence map›Paper›PMID 29547401›Full record

ReviewCurrent opinion in hematology2018

NOTCH regulation of the endothelial cell phenotype.

Julia J Mack, M Luisa Iruela-Arispe

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Matrix stiffness induces endothelial network senescence.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Induction of PD-1 and CD44 in CD4Journal of virology · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Another Notch in the Belt of Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Article

47 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

2 authors at 2 institutions in 2 countries.

Julia J MackDepartment of Molecular, Cell and Developmental Biology.
M Luisa Iruela-ArispeMolecular Biology Institute, University of California, Los Angeles, California, USA.
Institute of Molecular and Cell Biology · RUUniversity of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
NCI NIH HHS P30 CA016042NHLBI NIH HHS P01 HL030568
6 · The paper itself

Abstract

purpose of reviewThe formation of a hierarchical vascular network is a complex process that requires precise temporal and spatial integration of several signaling pathways. Amongst those, Notch has emerged as a key regulator of multiple steps that expand from endothelial sprouting to arterial specification and remains relevant in the adult. This review aims to summarize major concepts and rising hypotheses on the role of Notch signaling in the endothelium. RECENT

findingsA wealth of new information has helped to clarify how Notch signaling cooperates with other pathways to orchestrate vascular morphogenesis, branching, and function. Endothelial vascular endothelial growth factor, C-X-C chemokine receptor type 4, and nicotinamide adenine dinucleotide phosphate oxidase 2 have been highlighted as key regulators of the pathway. Furthermore, blood flow forces during vascular development induce Notch1 signaling to suppress endothelial cell proliferation, enhance barrier function, and promote arterial specification. Importantly, Notch1 has been recently recognized as an endothelial mechanosensor that is highly responsive to the level of shear stress to enable differential Notch activation in distinct regions of the vessel wall and suppress inflammation. SUMMARY: Although it is well accepted that the Notch signaling pathway is essential for vascular morphogenesis, its contributions to the homeostasis of adult endothelium were uncovered only recently. Furthermore, its exquisite regulation by flow and impressive interface with multiple signaling pathways indicates that Notch is at the center of a highly interactive web that integrates both physical and chemical signals to ensure vascular stability.

Indexed as

AnimalsBlood Flow VelocityCell ProliferationEndothelial CellsHumansMechanotransduction, CellularNADPH Oxidase 2Neovascularization, PhysiologicReceptor, Notch1Receptors, CXCR4Shear StrengthVascular Endothelial Growth Factor ACXCR4 protein, humanCYBB protein, humanNADPH Oxidase 2NOTCH1 protein, humanReceptor, Notch1Receptors, CXCR4Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID29547401
PMCPMC5902133
OpenAlexW2794403972

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.