Evidence map›Paper›PMID 26131974›Full record

ReviewBiomolecules2015

NF-kappaB Signaling in Chronic Inflammatory Airway Disease.

Michael Schuliga

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed, 2 pooled it
12.2field-weighted citation impact, top 1% 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

215 citing papers in PubMed, 2 syntheses or guidelines pooled it, 412 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Gngt2 promotes inflammatory dendritic cell programming through an ATG5-NF-κB signaling axis in neutrophilic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Identification ofInternational journal of chronic obstructive pulmonary disease · 2026
    Article
  14. Review
  15. Anti-Inflammatory Mechanisms and Translational Relevance ofJournal of inflammation research · 2026
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

155 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Michael SchuligaLung Health Research Centre (LHRC), Department Pharmacology and Therapeutics, University of Melbourne, Grattan St., Parkville 3010, Victoria, Australia. schuliga@unimelb.edu.au.
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are obstructive airway disorders which differ in their underlying causes and phenotypes but overlap in patterns of pharmacological treatments. In both asthma and COPD, oxidative stress contributes to airway inflammation by inducing inflammatory gene expression. The redox-sensitive transcription factor, nuclear factor (NF)-kappaB (NF-κB), is an important participant in a broad spectrum of inflammatory networks that regulate cytokine activity in airway pathology. The anti-inflammatory actions of glucocorticoids (GCs), a mainstay treatment for asthma, involve inhibition of NF-κB induced gene transcription. Ligand bound GC receptors (GRs) bind NF-κB to suppress the transcription of NF-κB responsive genes (i.e., transrepression). However, in severe asthma and COPD, the transrepression of NF-κB by GCs is negated as a consequence of post-translational changes to GR and histones involved in chromatin remodeling. Therapeutics which target NF-κB activation, including inhibitors of IκB kinases (IKKs) are potential treatments for asthma and COPD. Furthermore, reversing GR/histone acetylation shows promise as a strategy to treat steroid refractory airway disease by augmenting NF-κB transrepression. This review examines NF-κB signaling in airway inflammation and its potential as target for treatment of asthma and COPD.

Indexed as

Signal TransductionAsthmaGlucocorticoidsHumansMolecular Targeted TherapyNF-kappa BPulmonary Disease, Chronic ObstructiveRespiratory SystemGlucocorticoidsNF-kappa Bairway smooth muscleallergic asthmaalveolar macrophagescigarette smokeemphysemaeosinophilsepitheliumhistone deacetylasephosphoinositide 3 kinase-delta (PI3K-δ)sirtuins

Identifiers

PMID26131974
PMCPMC4598751
OpenAlexW1837564390

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.