Evidence map›Paper›PMID 18311158›Full record

ReviewBritish journal of pharmacology2008

Adenosine receptors and asthma.

R A Brown, D Spina, C P Page

Open access · greenAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
9.3field-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

48 citing papers in PubMed, 143 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. iScience · 2025
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. CD73: Friend or Foe in Lung Injury.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Discovery of a High Affinity Adenosine AACS medicinal chemistry letters · 2022
    Article
  16. Review
  17. Review
  18. Article
  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

3 authors at 1 institution in 1 country.

R A BrownKing's College London, Sackler Institute of Pulmonary Pharmacology, Division of Biomedical and Health Sciences, London, UK.
D Spina
C P Page
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of evidence implicating a role for adenosine in the pathogenesis of asthma has led to investigations into all adenosine receptor subtypes as potential therapeutic targets for the treatment of asthma. Selective A(1) receptor antagonists are currently in preclinical development since adenosine has been shown experimentally to mediate various features of asthma through this receptor such as bronchoconstriction, mucus secretion and inflammation. The A(2A) receptor is expressed on most inflammatory cells implicated in asthma, and as A(2A) stimulation activates adenylate cyclase and consequently elevates cAMP, selective A(2A) receptor agonists have now reached clinical development. However, initial reports concerning their efficacy are inconclusive. A(2B) receptor antagonists are also under investigation based on the rationale that inhibiting the effects of adenosine on mast cells would be beneficial, in addition to other reported pro-inflammatory effects mediated by the A(2B) receptor on cells such as airway smooth muscle, epithelial cells and fibroblasts. Whilst the effects in pre-clinical models are promising, their efficacy in the clinical setting has also yet to be reported. Finally, adenosine A(3) receptor stimulation has been demonstrated to mediate inhibitory effects on eosinophils since it also elevates cAMP. However, some experimental reports suggest that A(3) antagonists mediate anti-inflammatory effects, thus the rationale for A(3) receptor ligands as therapeutic agents remains to be determined. In conclusion, establishing the precise role of adenosine in the pathogenesis of asthma and developing appropriate subtype selective agonists/antagonists represents an exciting opportunity for the development of novel therapeutics for the treatment of asthma.

Indexed as

AdenosineAnimalsAnti-Asthmatic AgentsAsthmaBronchoconstrictionHumansInflammationReceptor, Adenosine A1Receptor, Adenosine A2AReceptor, Adenosine A3Receptors, Purinergic P1AdenosineAnti-Asthmatic AgentsReceptor, Adenosine A1Receptor, Adenosine A2AReceptor, Adenosine A3Receptors, Purinergic P1

Identifiers

PMID18311158
PMCPMC2268070
OpenAlexW1895752462

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.