Evidence map›Paper›PMID 20356986›Full record

ArticleThe European respiratory journal2010

Asthma and pulmonary arterial hypertension: do they share a key mechanism of pathogenesis?

S I Said, S A Hamidi, L Gonzalez Bosc

Open access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Targeting type-2 inflammation in pulmonary hypertension: lessons from a novel model.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Observational
  10. Article
  11. Article
  12. Resistin family proteins in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  13. Article
  14. miRNAs in Lung Development and Diseases.International journal of molecular sciences · 2020
    Review
  15. The role of CaScientific reports · 2020
    Article
  16. Review
  17. Article
  18. Pruning of the Pulmonary Vasculature in Asthma. The Severe Asthma Research Program (SARP) Cohort.American journal of respiratory and critical care medicine · 2018
    Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

S I SaidPulmonary and Critical Care Medicine, Stony Brook University, Stony Brook, NY 11794 , USA. sami.i.said@stonybrook.edu
S A Hamidi
L Gonzalez Bosc
Stony Brook University · USNorthport VA Medical Center · US

Funding

NFATc3 in chronic hypoxic pulmonary hypertensionR01HL088151 · NHLBI · UNIVERSITY OF NEW MEXICO · PI GONZALEZ BOSC, LAURA V · 2008 to 2012
$2.0M
Modulation of Lung Inflammation and Cell Death by VIPR01HL070212 · NHLBI · STATE UNIVERSITY NEW YORK STONY BROOK · PI SAID, SAMI I · 2002 to 2006
$941k
NHLBI NIH HHS HL-70212NHLBI NIH HHS HL-88151NHLBI NIH HHS R01 HL070212NHLBI NIH HHS R01 HL088151
6 · The paper itself

Abstract

Although largely distinct and seemingly unrelated, asthma and pulmonary arterial hypertension (PAH) have important pathological features in common, including inflammation, smooth muscle contraction and remodelling. We hypothesised that these common features could be explained by one shared mechanism of pathogenesis: activation of the transcription factor NFAT (nuclear factor of activated T-cells). If this concept is validated, it could lead to the introduction of novel therapeutic strategies against both lung disorders. In several experimental models, airway remodelling is accompanied by remodelling of smaller pulmonary arteries, validating the hypothesis of their similar pathogenesis. In addition, lungs of vasoactive intestinal peptide (VIP) knockout mice express airway hyperresponsiveness with airway inflammation and PAH with vascular remodelling, with both sets of pathological findings being reversible with VIP treatment. Preliminary data suggest that absence of the VIP gene leads to activation of the calcineurin-NFAT pathway, and that VIP is probably a physiological inhibitor of this pathway. Enough evidence exists to support the views that asthma and PAH share important pathological features, probably related to NFAT activation, and that VIP may be a physiological modulator of this mechanism.

Indexed as

AsthmaCalcineurinHumansHypertension, PulmonaryMuscle, Smooth, VascularNFATC Transcription FactorsPneumoniaPulmonary ArterySignal TransductionCalcineurinNFATC Transcription Factors

Identifiers

PMID20356986
PMCPMC2963099
OpenAlexW2138452463

What OpenQuestion holds

Textmetadata
LicenceTDM
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.