Evidence map›Paper›PMID 34681953›Full record

ArticleInternational journal of molecular sciences2021

ELTD1 Activation Induces an Endothelial-EMT Transition to a Myofibroblast Phenotype.

Helen Sheldon, John Alexander, Esther Bridges, Lucia Moreira, Svetlana Reilly, Koon Hwee Ang, Dian Wang, Salwa Lin, Syed Haider, Alison H Banham and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  3. Article
  4. Structure of the GNature communications · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
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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 1 country.

Helen SheldonCancer Research UK Molecular Oncology Laboratories, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.ORCID 0000-0002-0945-5496
John AlexanderThe Breast Cancer Now Toby Robins Research Centre, Division of Breast Cancer Research, The Institute of Cancer Research, London SM2 5NG, UK.
Esther BridgesCancer Research UK Molecular Oncology Laboratories, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Lucia MoreiraCardiovascular Medicine, RDM John Radcliffe Hospital, Oxford OX3 9DU, UK.ORCID 0000-0001-8168-1538
Svetlana ReillyCardiovascular Medicine, RDM John Radcliffe Hospital, Oxford OX3 9DU, UK.
Koon Hwee AngCancer Research UK Molecular Oncology Laboratories, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.ORCID 0000-0002-0321-1992
Dian WangNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Salwa LinCancer Research UK Molecular Oncology Laboratories, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Syed HaiderThe Breast Cancer Now Toby Robins Research Centre, Division of Breast Cancer Research, The Institute of Cancer Research, London SM2 5NG, UK.ORCID 0000-0001-6685-5480
Alison H BanhamNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Adrian L HarrisCancer Research UK Molecular Oncology Laboratories, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.ORCID 0000-0003-1376-8409
Cancer Research UK · GBJohn Radcliffe Hospital · GBInstitute of Cancer Research · GB

Funding

British Heart Foundation FS/16/5/32054British Heart Foundation FS/20/7/34992Cancer Research UK 11359Cancer Research UK 18974Cancer Research UK C602/A18974Wellcome Trust
6 · The paper itself

Abstract

ELTD1 is expressed in endothelial and vascular smooth muscle cells and has a role in angiogenesis. It has been classified as an adhesion GPCR, but as yet, no ligand has been identified and its function remains unknown. To establish its role, ELTD1 was overexpressed in endothelial cells. Expression and consequently ligand independent activation of ELTD1 results in endothelial-mesenchymal transistion (EndMT) with a loss of cell-cell contact, formation of stress fibres and mature focal adhesions and an increased expression of smooth muscle actin. The effect was pro-angiogenic, increasing Matrigel network formation and endothelial sprouting. RNA-Seq analysis after the cells had undergone EndMT revealed large increases in chemokines and cytokines involved in regulating immune response. Gene set enrichment analysis of the data identified a number of pathways involved in myofibroblast biology suggesting that the endothelial cells had undergone a type II EMT. This type of EMT is involved in wound repair and is closely associated with inflammation implicating ELTD1 in these processes.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression RegulationNeovascularization, PathologicAnimalsApoptosisBiomarkersCell MovementCell ProliferationCells, CulturedEndothelial CellsHumansMiceMice, Inbred C57BLMyofibroblastsPhenotypeReceptors, G-Protein-CoupledADGRL4 protein, humanBiomarkersReceptors, G-Protein-CoupledELTD1EMTmyofibroblastpro-angiogenic

Identifiers

PMID34681953
PMCPMC8539764
OpenAlexW3206999213

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.