Evidence map›Paper›PMID 22052929›Full record

ReviewProceedings of the American Thoracic Society2011

Studies of vascular endothelial growth factor in asthma and chronic obstructive pulmonary disease.

Chun Geun Lee, Bing Ma, Seyedtaghi Takyar, Farida Ahangari, Charles Delacruz, Chuan Hua He, Jack A Elias

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.3field-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

47 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. ETERJ open research · 2026
    Article
  4. Hyperconcentrated mucus in small airways: a mechanistic model for the pathogenesis of paediatric bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Fungal Aeroallergens-The Impact of Climate Change.Journal of fungi (Basel, Switzerland) · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Resident mesenchymal vascular progenitors modulate adaptive angiogenesis and pulmonary remodeling via regulation of canonical Wnt signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    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

7 authors at 1 institution in 1 country.

Chun Geun LeeSection of Pulmonary and Critical Care Medicine, Yale University School of Medicine, Department of Internal Medicine, New Haven, Connecticut, USA.
Bing Ma
Seyedtaghi Takyar
Farida Ahangari
Charles Delacruz
Chuan Hua He
Jack A Elias
Yale University · US

Funding

Preotease/Cathepsin-Mediated Apoptosis in COPDR01HL079328 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2005 to 2012
$3.2M
NHLBI NIH HHS HL-079328NHLBI NIH HHS R01 HL079328
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) is a potent stimulator of vascular angiogenesis, permeability, and remodeling that also plays important roles in wound healing and tissue cytoprotection. To begin to define the roles of VEGF in diseases like asthma and COPD, we characterized the effects of lung-targeted transgenic VEGF(165) and defined the innate immune pathways that regulate VEGF tissue responses. The former studies demonstrated that VEGF plays an important role in Th2 inflammation because, in addition to stimulating angiogenesis and edema, VEGF induced eosinophilic inflammation, mucus metaplasia, subepithelial fibrosis, myocyte hyperplasia, dendritic cell activation, and airways hyperresponsiveness via IL-13-dependent and -independent mechanisms. VEGF was also produced at sites of aeroallergen-induced Th2 inflammation, and VEGF receptor blockade ameliorated adaptive Th2 inflammation and Th2 cytokine elaboration. The latter studies demonstrated that activation of the RIG-like helicase (RLH) innate immune pathway using viral pathogen-associated molecular patterns such as Poly(I:C) or viruses ameliorated VEGF-induced tissue responses. In accord with these findings, Poly(I:C)-induced RLH activation also abrogated aeroallergen-induced Th2 inflammation. When viewed in combination, these studies suggest that VEGF excess can contribute to the pathogenesis of Th2 inflammatory disorders such as asthma and that abrogation of VEGF signaling via RLH activation can contribute to the pathogenesis of viral disorders such as virus-induced COPD exacerbations. They also suggest that RLH activation may be a useful therapeutic strategy in asthma and related disorders.

Indexed as

AnimalsAsthmaDisease Models, AnimalHumansInflammationMicePulmonary Disease, Chronic ObstructiveVascular Endothelial Growth Factor AVascular Endothelial Growth Factor A

Identifiers

PMID22052929
PMCPMC3359071
OpenAlexW2103871834

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.