Evidence map›Paper›PMID 28661183›Full record

ArticleAmerican journal of respiratory and critical care medicine2017

Differential Expression of VEGF-A

Shaney L Barratt, Thomas Blythe, Caroline Jarrett, Khadija Ourradi, Golda Shelley-Fraser, Michael J Day, Yan Qiu, Steve Harper, Toby M Maher, Sebastian Oltean and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

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  14. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 3 countries.

Shaney L Barratt1 Academic Respiratory Unit, School of Clinical Sciences.
Thomas Blythe1 Academic Respiratory Unit, School of Clinical Sciences.
Caroline Jarrett1 Academic Respiratory Unit, School of Clinical Sciences.
Khadija Ourradi1 Academic Respiratory Unit, School of Clinical Sciences.
Golda Shelley-Fraser2 Department of Histopathology, Cheltenham and Gloucestershire NHS Trust, Cheltenham, United Kingdom.
Michael J Day3 School of Veterinary Sciences.
Yan Qiu4 Academic Renal Unit, and.
Steve Harper4 Academic Renal Unit, and.
Toby M Maher5 NIHR Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom.
Sebastian Oltean6 Department of Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom.
Thomas J Hames7 University of Exeter Medical School, Exeter, United Kingdom; and.
Chris J Scotton7 University of Exeter Medical School, Exeter, United Kingdom; and.
Gavin I Welsh4 Academic Renal Unit, and.
David O Bates8 Cancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Ann B Millar1 Academic Respiratory Unit, School of Clinical Sciences.
At Bristol · GBRenal Association · GBUniversity of Bristol · GBUniversity of Exeter · GBRoyal Brompton Hospital · GBUniversity of Nottingham · GB

Funding

British Heart Foundation PG/15/53/31371Medical Research Council G10002073Medical Research Council MR/K020366/1Wellcome TrustWellcome Trust 95114
6 · The paper itself

Abstract

rationaleFibrosis after lung injury is related to poor outcome, and idiopathic pulmonary fibrosis (IPF) can be regarded as an exemplar. Vascular endothelial growth factor (VEGF)-A has been implicated in this context, but there are conflicting reports as to whether it is a contributory or protective factor. Differential splicing of the VEGF-A gene produces multiple functional isoforms including VEGF-A

objectivesTo establish VEGF-A isoform expression and functional effects in IPF.

methodsWe used tissue sections, plasma, and lung fibroblasts from patients with IPF and control subjects. In a bleomycin-induced lung fibrosis model we used wild-type MMTV mice and a triple transgenic mouse SPC-rtTA MEASUREMENTS AND MAIN

resultsIPF and normal lung fibroblasts differentially expressed and responded to VEGF-A

conclusionsThese results indicate that changes in the bioavailability of VEGF-A sourced from ATII cells, namely the ratio of VEGF-A

Indexed as

AnimalsDisease Models, AnimalGene ExpressionHumansLungMiceMice, Inbred C57BLProtein IsoformsPulmonary FibrosisVascular Endothelial Growth Factor AProtein IsoformsVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVEGFA protein, humananimal models of pulmonary fibrosisidiopathic pulmonary fibrosisvascular endothelial growth factor

Identifiers

PMID28661183
PMCPMC5564672
OpenAlexW2728152280

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.