Evidence map›Paper›PMID 20971733›Full record

ArticleThe American journal of pathology2010

Protease-activated receptor-2 induces myofibroblast differentiation and tissue factor up-regulation during bleomycin-induced lung injury: potential role in pulmonary fibrosis.

Keren Borensztajn, Paul Bresser, Chris van der Loos, Ilze Bot, Bernt van den Blink, Michael A den Bakker, Joost Daalhuisen, Angelique P Groot, Maikel P Peppelenbosch, Jan H von der Thüsen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  9. Airway Resistance Caused by Sphingomyelin Synthase 2 Insufficiency in Response to Cigarette Smoke.American journal of respiratory cell and molecular biology · 2020
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  10. Article
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  16. Membrane-anchored Serine Protease Matriptase Is a Trigger of Pulmonary Fibrogenesis.American journal of respiratory and critical care medicine · 2016
    Article
  17. Article
  18. Article
  19. Thy1 (CD90) controls adipogenesis by regulating activity of the Src family kinase, Fyn.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  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

11 authors at 4 institutions in 4 countries.

Keren BorensztajnCenter for Experimental and Molecular Medicine, Academic Medical Center, Meibergdreef 9, NL-1105 AZ, Amsterdam, The Netherlands. K.S.Borensztajn@amc.uva.nl
Paul Bresser
Chris van der Loos
Ilze Bot
Bernt van den Blink
Michael A den Bakker
Joost Daalhuisen
Angelique P Groot
Maikel P Peppelenbosch
Jan H von der Thüsen
C Arnold Spek
Amsterdam UMC Location University of Amsterdam · NLErasmus MC · NLUniversity of Groningen · NLLeiden University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis constitutes the most devastating form of fibrotic lung disorders and remains refractory to current therapies. The coagulation cascade is frequently activated during pulmonary fibrosis, but this observation has so far resisted a mechanistic explanation. Recent data suggest that protease-activated receptor (PAR)-2, a receptor activated by (among others) coagulation factor (F)Xa, plays a key role in fibrotic disease; consequently, we assessed the role of PAR-2 in the development of pulmonary fibrosis in this study. We show that PAR-2 is up-regulated in the lungs of patients with idiopathic pulmonary fibrosis and that bronchoalveolar lavage fluid from these patients displays increased procoagulant activity that triggers fibroblast survival. Using a bleomycin model of pulmonary fibrosis, we show that bleomycin induces PAR-2 expression, as well as both myofibroblast differentiation and collagen synthesis. In PAR-2-/- mice, both the extent and severity of fibrotic lesions are reduced, whereas myofibroblast differentiation is diminished and collagen expression is decreased. Moreover, fibrin deposition in the lungs of fibrotic PAR-2-/- mice is reduced compared with wild-type mice due to differential tissue factor expression in response to bleomycin. Taken together, these results suggest an important role for PAR-2 in the development of pulmonary fibrosis, and the inhibition of the PAR-2-coagulation axis may provide a novel therapeutic approach to treat this devastating disease.

Indexed as

AdultAgedAnimalsBleomycinCell DifferentiationCells, CulturedHumansLung InjuryMiceMice, Inbred C57BLMice, KnockoutMiddle AgedMyofibroblastsPulmonary FibrosisReceptor, PAR-2ThromboplastinBleomycinReceptor, PAR-2Thromboplastin

Identifiers

PMID20971733
PMCPMC2993271
OpenAlexW1541546534

What OpenQuestion holds

Textmetadata
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.