Evidence map›Paper›PMID 31974352›Full record

ArticleNature communications2020

Non-canonical Wnt signalling regulates scarring in biliary disease via the planar cell polarity receptors.

D H Wilson, E J Jarman, R P Mellin, M L Wilson, S H Waddell, P Tsokkou, N T Younger, A Raven, S R Bhalla, A T R Noll and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Wnt signaling in biliary development, proliferation, and fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Monomeric/dimeric forms of Fgf15/FGF19 show differential activity in hepatocyte proliferation and metabolic function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  19. Fibrocystic liver disease: novel concepts and translational perspectives.Translational gastroenterology and hepatology · 2021
    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

20 authors at 11 institutions in 6 countries.

D H WilsonMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.ORCID http://orcid.org/0000-0001-8322-0380
E J JarmanMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.ORCID http://orcid.org/0000-0002-5466-4430
R P MellinMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.ORCID http://orcid.org/0000-0002-4567-0660
M L WilsonMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.
S H WaddellMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.
P TsokkouMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.ORCID http://orcid.org/0000-0001-8095-2615
N T YoungerMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK.ORCID http://orcid.org/0000-0001-7601-9283
A RavenCancer Research UK Beatson Institute, Glasgow, UK.
S R BhallaCancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Centre for Cancer Science, Queen's Medical Centre, Nottingham, UK.
A T R NollDepartment of Surgery, Maastricht University, Maastricht, The Netherlands.
S W Olde DaminkDepartment of Surgery, Maastricht University, Maastricht, The Netherlands.
F G SchaapDepartment of Surgery, Maastricht University, Maastricht, The Netherlands.
P ChenDepartment of Cell Biology, Emory University School of Medicine, Atlanta, GA, 30322, USA.
D O BatesCancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Centre for Cancer Science, Queen's Medical Centre, Nottingham, UK.
J M BanalesBiodonostia HRI, CIBERehd, Ikerbasque, San Sebastian, Spain.
C H DeanNational Heart and Lung Institute, Imperial College London, London, UK.ORCID http://orcid.org/0000-0002-8846-5472
D J HendersonCardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle, UK.
O J SansomCancer Research UK Beatson Institute, Glasgow, UK.ORCID http://orcid.org/0000-0001-9540-3010
T J KendallUniversity of Edinburgh Centre for Inflammation Research, Edinburgh, UK.ORCID http://orcid.org/0000-0002-4174-2786
L BoulterMRC Human Genetics Unit, Institute for Genetic and Molecular Medicine, Edinburgh, UK. luke.boulter@ed.ac.uk.ORCID http://orcid.org/0000-0002-7954-6705
Institute of Genetics and Cancer · GBMaastricht University · NLCancer Research UK Scotland Institute · GBBirmingham City University · GBCentre for Inflammation Research · GBEmory University · USIkerbasque · ESImperial College London · GBNewcastle University · GBUniversity of Nottingham · GBWalter and Eliza Hall Institute of Medical Research · AU

Funding

British Heart Foundation PG/11/76/29108Cancer Research UK 21139Cancer Research UK 26813Wellcome Trust
6 · The paper itself

Abstract

The number of patients diagnosed with chronic bile duct disease is increasing and in most cases these diseases result in chronic ductular scarring, necessitating liver transplantation. The formation of ductular scaring affects liver function; however, scar-generating portal fibroblasts also provide important instructive signals to promote the proliferation and differentiation of biliary epithelial cells. Therefore, understanding whether we can reduce scar formation while maintaining a pro-regenerative microenvironment will be essential in developing treatments for biliary disease. Here, we describe how regenerating biliary epithelial cells express Wnt-Planar Cell Polarity signalling components following bile duct injury and promote the formation of ductular scars by upregulating pro-fibrogenic cytokines and positively regulating collagen-deposition. Inhibiting the production of Wnt-ligands reduces the amount of scar formed around the bile duct, without reducing the development of the pro-regenerative microenvironment required for ductular regeneration, demonstrating that scarring and regeneration can be uncoupled in adult biliary disease and regeneration.

Indexed as

Wnt Signaling PathwayAnimalsAxin ProteinBile Duct DiseasesBile DuctsCell PolarityCholangitis, SclerosingCicatrixDisease Models, AnimalEpithelial CellsHumansJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Kinase 4Mice, TransgenicNerve Tissue Proteins3,5-diethoxycarbonyl-1,4-dihydrocollidineAXIN2 protein, humanAxin2 protein, mouseAxin ProteinJNK Mitogen-Activated Protein KinasesLtap protein, mouseMAP Kinase Kinase 4Nerve Tissue ProteinsPyridinesWnt-5a Protein

Identifiers

PMID31974352
PMCPMC6978415
OpenAlexW3002436408

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.