Evidence map›Paper›PMID 27846380›Full record

ArticleThe American journal of pathology2017

Pulmonary Vasculopathy Associated with FIGF Gene Mutation.

Evan Bailey, Ye Cui, Alicia Casey, Joan M Stoler, Xingbin Ai, Dongdong Ma, Robert Handin, Piotr Sliz, Sara O Vargas, Souheil Y El-Chemaly

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Lymphatic Changes in Respiratory Diseases: More than Just Remodeling of the Lung?American journal of respiratory cell and molecular biology · 2017
    Review
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

10 authors at 3 institutions in 1 country.

Evan BaileyDivision of Pulmonary Medicine, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Ye CuiDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Alicia CaseyDivision of Pulmonary Medicine, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Joan M StolerDivision of Genetics and Genomics, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Xingbin AiDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Dongdong MaDivision of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Robert HandinDivision of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Piotr SlizDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts.
Sara O VargasDepartment of Pathology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Souheil Y El-ChemalyDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: sel-chemaly@partners.org.
Harvard University · USBrigham and Women's Hospital · USBoston Children's Hospital · US

Funding

Effects of lymphangiogenesis stimulation on lung allograft rejectionR21HL119902 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI EL-CHEMALY, SOUHEIL · 2013 to 2014
$444k
NHLBI NIH HHS R21 HL119902
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF)-D is capable of inducing angiogenesis and lymphangiogenesis through signaling via VEGF receptor (VEGFR)-2 and VEGFR-3, respectively. Mutations in the FIGF (c-fos-induced growth factor) gene encoding VEGF-D have not been reported previously. We describe a young male with a hemizygous mutation in the X-chromosome gene FIGF (c.352 G>A) associated with early childhood respiratory deficiency. Histologically, lungs showed ectatic pulmonary arteries and pulmonary veins. The mutation resulted in a substitution of valine to methionine at residue 118 of the VEGF-D protein. The resultant mutant protein had increased dimerization, induced elevated VEGFR-2 signaling, and caused aberrant angiogenesis in vivo. Our observations characterize a new subtype of congenital diffuse lung disease, provide a histological correlate, and support a critical role for VEGF-D in lung vascular development and homeostasis.

Indexed as

Genetic Predisposition to DiseaseAnimalsCell LineChickensChildChild, PreschoolFamilyHumansInfantInfant, NewbornLungLung DiseasesMaleMutationNeovascularization, PathologicVascular DiseasesVascular Endothelial Growth Factor DVEGFD protein, human

Identifiers

PMID27846380
PMCPMC5225300
OpenAlexW2553980432

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.