Evidence map›Paper›PMID 26308618›Full record

ArticleAmerican journal of respiratory and critical care medicine2015

Hepatic Shunting of Eggs and Pulmonary Vascular Remodeling in Bmpr2(+/-) Mice with Schistosomiasis.

Alexi Crosby, Elaine Soon, Frances M Jones, Mark R Southwood, Leila Haghighat, Mark R Toshner, Tim Raine, Ian Horan, Peiran Yang, Stephen Moore and 7 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Schistosomiasis-associated pulmonary arterial hypertension: a systematic review.European respiratory review : an official journal of the European Respiratory Society · 2020
    Pooled it
  2. Article
  3. Review
  4. ExperimentalPulmonary circulation · 2024
    Article
  5. Article
  6. Article
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  8. Review
  9. Article
  10. Article
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  14. The Role of Type 2 Inflammation inFrontiers in immunology · 2019
    Review
  15. Article
  16. Article
  17. HIF2α-arginase axis is essential for the development of pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  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

17 authors at 4 institutions in 2 countries.

Alexi Crosby1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.ORCID http://orcid.org/0000-0001-5063-961X
Elaine Soon1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Frances M Jones2 Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
Mark R Southwood3 Department of Pathology, Papworth Hospital, Cambridge, United Kingdom.
Leila Haghighat1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Mark R Toshner1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Tim Raine1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Ian Horan1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Peiran Yang1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Stephen Moore1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Elisabet Ferrer1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
Penny Wright4 Addenbrooke's Hospital, Cambridge, United Kingdom; and.
Mark L Ormiston1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
R James White5 University of Rochester, Rochester, New York.
Deborah A Haight5 University of Rochester, Rochester, New York.
David W Dunne2 Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
Nicholas W Morrell1 Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom.
University of Cambridge · GBUniversity of Rochester · USAddenbrooke's Hospital · GBPapworth Hospital · GB

Funding

British Heart Foundation FS/12/39/29653British Heart Foundation PG/10/35/28339British Heart Foundation PG/13/91/30579Medical Research Council G0802261Wellcome TrustWellcome Trust 096822/Z/11/Z
6 · The paper itself

Abstract

rationaleSchistosomiasis is a major cause of pulmonary arterial hypertension (PAH). Mutations in the bone morphogenetic protein type-II receptor (BMPR-II) are the commonest genetic cause of PAH.

objectivesTo determine whether Bmpr2(+/-) mice are more susceptible to schistosomiasis-induced pulmonary vascular remodeling.

methodsWild-type (WT) and Bmpr2(+/-) mice were infected percutaneously with Schistosoma mansoni. At 17 weeks postinfection, right ventricular systolic pressure and liver and lung egg counts were measured. Serum, lung and liver cytokine, pulmonary vascular remodeling, and liver histology were assessed. MEASUREMENTS AND MAIN

resultsBy 17 weeks postinfection, there was a significant increase in pulmonary vascular remodeling in infected mice. This was greater in Bmpr2(+/-) mice and was associated with an increase in egg deposition and cytokine expression, which induced pulmonary arterial smooth muscle cell proliferation, in the lungs of these mice. Interestingly, Bmpr2(+/-) mice demonstrated dilatation of the hepatic central vein at baseline and postinfection, compared with WT. Bmpr2(+/-) mice also showed significant dilatation of the liver sinusoids and an increase in inflammatory cells surrounding the central hepatic vein, compared with WT. This is consistent with an increase in the transhepatic passage of eggs.

conclusionsThis study has shown that levels of BMPR-II expression modify the pulmonary vascular response to chronic schistosomiasis. The likely mechanism involves the increased passage of eggs to the lungs, caused by altered diameter of the hepatic veins and sinusoids in Bmpr2(+/-) mice. Genetically determined differences in the remodeling of hepatic vessels may represent a new risk factor for PAH associated with schistosomiasis.

Indexed as

Bone Morphogenetic Protein Receptors, Type IIAnimalsCell ProliferationDisease Models, AnimalFemaleHypertension, PulmonaryLiverMicePulmonary ArterySchistosoma mansoniSchistosomiasisSignal TransductionVascular RemodelingBmpr2 protein, mouseBone Morphogenetic Protein Receptors, Type IIbone-morphogenetic protein type II receptorpulmonary hypertensionpulmonary vascular remodelingschistosomiasis

Identifiers

PMID26308618
PMCPMC4731697
OpenAlexW2170132609

What OpenQuestion holds

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Registered trials

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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.