Evidence map›Paper›PMID 28814671›Full record

ArticleJCI insight2017

Antifibrotic role of vascular endothelial growth factor in pulmonary fibrosis.

Lynne A Murray, David M Habiel, Miriam Hohmann, Ana Camelo, Huilan Shang, Yang Zhou, Ana Lucia Coelho, Xueyan Peng, Mridu Gulati, Bruno Crestani and 12 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 82 citations in OpenAlex.

  1. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  2. Article
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  4. Article
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  6. Article
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  9. Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025
    Review
  10. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Lung Immune Cell Niches and the Discovery of New Cell Subtypes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  15. Article
  16. Review
  17. Article
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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

22 authors at 8 institutions in 5 countries.

Lynne A MurrayMedImmune Ltd., Cambridge, England, United Kingdom.
David M HabielDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Miriam HohmannDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Ana CameloMedImmune Ltd., Cambridge, England, United Kingdom.
Huilan ShangDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Yang ZhouYale University School of Medicine, New Haven, Connecticut, USA.
Ana Lucia CoelhoDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Xueyan PengYale University School of Medicine, New Haven, Connecticut, USA.
Mridu GulatiYale University School of Medicine, New Haven, Connecticut, USA.
Bruno CrestaniAPHP, Hôpital Bichat, Service de Pneumologie A, Centre de Compétences des Maladies Pulmonaires Rares, Paris, France Université Paris Diderot, Sorbonne Paris Cité, INSERM Unité 1152, Paris.
Matthew A SleemanMedImmune Ltd., Cambridge, England, United Kingdom.
Tomas MustelinMedImmune LLC., Gaithersburg, Maryland, USA.
Meagan W MooreYale University School of Medicine, New Haven, Connecticut, USA.
Changwan RyuYale University School of Medicine, New Haven, Connecticut, USA.
Awo D Osafo-AddoYale University School of Medicine, New Haven, Connecticut, USA.
Jack A EliasWarren Alpert School of Medicine, Providence, Rhode Island, USA.
Chun G LeeWarren Alpert School of Medicine, Providence, Rhode Island, USA.
Buqu HuYale University School of Medicine, New Haven, Connecticut, USA.
Jose D Herazo-MayaYale University School of Medicine, New Haven, Connecticut, USA.
Darryl A KnightViva program, Hunter Medical Research Institute, Newcastle, NSW, Australia.
Cory M HogaboamDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Erica L HerzogYale University School of Medicine, New Haven, Connecticut, USA.
Yale University · USCedars-Sinai Medical Center · USAimmune Therapeutics (United Kingdom) · GBBrown University · USAltimmune (United States) · USInserm · FRUniversity of British Columbia · CAUniversity of Michigan · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Novel Immunologic Effects of Semaphorin 7a in IPFR01HL109233 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2011 to 2019
$3.7M
Innate DNA sensing in rapidly progressing IPFR01HL123899 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI HOGABOAM, CORY M · 2015 to 2018
$2.0M
Neuroimmune Molecules in Scleroderma Lung FibrosisR01HL125850 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2016 to 2019
$1.7M
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL109233NHLBI NIH HHS R01 HL123899NHLBI NIH HHS R01 HL125850
6 · The paper itself

Abstract

The chronic progressive decline in lung function observed in idiopathic pulmonary fibrosis (IPF) appears to result from persistent nonresolving injury to the epithelium, impaired restitution of the epithelial barrier in the lung, and enhanced fibroblast activation. Thus, understanding these key mechanisms and pathways modulating both is essential to greater understanding of IPF pathogenesis. We examined the association of VEGF with the IPF disease state and preclinical models in vivo and in vitro. Tissue and circulating levels of VEGF were significantly reduced in patients with IPF, particularly in those with a rapidly progressive phenotype, compared with healthy controls. Lung-specific overexpression of VEGF significantly protected mice following intratracheal bleomycin challenge, with a decrease in fibrosis and bleomycin-induced cell death observed in the VEGF transgenic mice. In vitro, apoptotic endothelial cell-derived mediators enhanced epithelial cell injury and reduced epithelial wound closure. This process was rescued by VEGF pretreatment of the endothelial cells via a mechanism involving thrombospondin-1 (TSP1). Taken together, these data indicate beneficial roles for VEGF during lung fibrosis via modulating epithelial homeostasis through a previously unrecognized mechanism involving the endothelium.

Indexed as

InflammationPulmonology

Identifiers

PMID28814671
PMCPMC5621899
OpenAlexW2748216636

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.