Evidence map›Paper›PMID 24773466›Full record

ReviewAllergy2014

Refractory asthma: mechanisms, targets, and therapy.

J L Trevor, J S Deshane

Open access · bronzeAbstract readReview
In one paragraph

Review in Allergy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 132 citations in OpenAlex.

  1. Trial
  2. Trial
  3. MrgprC11American journal of respiratory cell and molecular biology · 2025
    Article
  4. Article
  5. Review
  6. Distinctive CD39Nature communications · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Significance of Singlet Oxygen Molecule in Pathologies.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Article
  13. Glucocorticoids and COVID-19.Pharmacological research · 2022
    Review
  14. RNA-Binding Protein HuR Promotes Airway Inflammation in a House Dust Mite-Induced Allergic Asthma Model.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

J L TrevorDivision of Pulmonary Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
J S Deshane
University of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a common medical condition affecting 300 million people worldwide. Airway inflammation, smooth muscle bronchoconstriction leading to airflow obstruction, and mucous hypersecretion are clinical hallmarks of asthma. The NHLBI Expert Panel Report 3 recommends inhaled corticosteroids (ICS) for patients with moderate to severe persistent asthma. Inhaled corticosteroids (ICS) target gene transcription through their interactions with the glucocorticoid (GC) receptor (GR) at the glucocorticoid response element (GRE). The GC/GR complex enhances anti-inflammatory but inhibits pro-inflammatory mediator production. Classically, asthma has been described as a Th2-associated eosinophil-predominant disease, but recently alternative models have been described including a Th17-mediated neutrophil-predominant phenotype resulting in patients with more severe disease who may be less responsive to steroids. Additional mechanisms of steroid resistance include increased activity of GR phosphorylating kinases which modify the interactions of GR with transcription factors to inhibit the ability of GR to bind with GRE, leading to an increase in pro-inflammatory gene transcription. Oxidative stress also affects the balance between pro-inflammatory and anti-inflammatory gene transcription through the modification of transcription factors and cofactors (such as PI3K) leading to the inhibition of histone deacetylase 2. Continued investigations into the mechanisms behind glucocorticoid resistance will lead to novel treatments that improve control of severe refractory asthma.

Indexed as

Adrenal Cortex HormonesAnti-Asthmatic AgentsAsthmaDrug ResistanceHumansInflammationAdrenal Cortex HormonesAnti-Asthmatic Agentsasthmaglucocorticoidsoxidative stressrefractorysteroid resistance

Identifiers

PMID24773466
PMCPMC4279947
OpenAlexW2057930810

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.