Evidence map›Paper›PMID 26997628›Full record

ArticlePhysiological reports2016

Aberrant nonfibrotic parenchyma in idiopathic pulmonary fibrosis is correlated with decreased β-catenin inhibition and increased Wnt5a/b interaction.

Kristina Rydell-Törmänen, Xiao-Hong Zhou, Oskar Hallgren, Jonas Einarsson, Leif Eriksson, Annika Andersson-Sjöland, Gunilla Westergren-Thorsson

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Lung extracellular matrix modulates KRT5Nature communications · 2023
    Article
  4. Article
  5. Article
  6. Noncanonical Wnt Signaling Promotes Myofibroblast Differentiation in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021
    Article
  7. Article
  8. Idiopathic Pulmonary Comorbidities and Mechanisms.International journal of inflammation · 2021
    Review
  9. WNT Signalling in Lung Physiology and Pathology.Handbook of experimental pharmacology · 2021
    Article
  10. Observational
  11. The Wnt Signaling Pathway and the Development of Bronchopulmonary Dysplasia.American journal of respiratory and critical care medicine · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Thorax · 2017
    Review
  16. Article
  17. Distinct Roles of Wnt/Mediators of inflammation · 2017
    Review
  18. 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

7 authors at 2 institutions in 1 country.

Kristina Rydell-TörmänenLung Biology, Department Experimental Medical Science, Lund University, Lund, Sweden kristina.rydell-tormanen@med.lu.se.
Xiao-Hong ZhouDepartment of BioSciences, RIA iMed, AstraZeneca R&D Gothenburg, Mölndal, Sweden.
Oskar HallgrenLung Biology, Department Experimental Medical Science, Lund University, Lund, Sweden Respiratory Medicine and Allergology, Department Clinical Sciences, Lund University, Lund, Sweden.
Jonas EinarssonRespiratory Medicine and Allergology, Department Clinical Sciences, Lund University, Lund, Sweden Department Respiratory Medicine and Allergology, Skåne University Hospital, Lund, Sweden.
Leif ErikssonLung Biology, Department Experimental Medical Science, Lund University, Lund, Sweden Respiratory Medicine and Allergology, Department Clinical Sciences, Lund University, Lund, Sweden.
Annika Andersson-SjölandLung Biology, Department Experimental Medical Science, Lund University, Lund, Sweden.
Gunilla Westergren-ThorssonLung Biology, Department Experimental Medical Science, Lund University, Lund, Sweden.
Lund University · SEAstraZeneca (Sweden) · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF), an insidious disease with grave prognosis, is characterized by heterogeneous fibrosis with densely fibrotic areas surrounded by nonfibrotic normal-looking tissue, believed to reflect a temporal development. The etiology is incompletely elucidated, but aberrant wound healing is believed to be involved. Embryonic signaling pathways, including Wnt signaling, are reactivated in wound healing, and we therefore aimed to investigate Wnt signaling, and hypothesized that Wnt signaling would correspond to degree of fibrosis. Material from 10 patients with IPF were included (four diagnostic biopsies and six donated lungs) and compared to healthy controls (n = 7). We investigated markers of Wnt signaling (β-catenin, Wnt3a, ICAT, Wnt5a/b, DAAM1 and NLK) histologically in lung parenchyma with variable degree of fibrosis. Our results suggest that Wnt signaling is significantly altered (P < 0.05) already in normal-looking parenchyma. The expression of Wnt3a and ICAT decreased (both P < 0.01) in IPF compared to healthy lungs, whereas β-catenin, Wnt5a/b, DAAM1 and NLK increased (P < 0.05 for all). ICAT is further decreased in dense fibrosis compared to normal-looking parenchyma in IPF (P < 0.001). On the basis of our results, we conclude that from a Wnt perspective, there is no normal parenchyma in IPF, and Wnt signaling corresponds to degree of fibrosis. In addition, β-catenin and Wnt5a appears coupled, and decreased inhibition of β-catenin may be involved. We suggest that the interaction between β-catenin, ICAT, and Wnt5a/b may represent an important research area and potential target for therapeutic intervention.

Indexed as

AdultAgedAged, 80 and overbeta CateninFemaleHumansIdiopathic Pulmonary FibrosisLungMaleMiddle AgedProtein BindingProto-Oncogene ProteinsWnt-5a ProteinWnt Proteinsbeta CateninCTNNB1 protein, humanProto-Oncogene ProteinsWnt-5a ProteinWNT5A protein, humanWNT5B protein, humanWnt ProteinsICATidiopathic pulmonary fibrosisWnt5aWnt signalingβ‐catenin

Identifiers

PMID26997628
PMCPMC4823602
OpenAlexW2303744950

What OpenQuestion holds

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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.