Evidence map›Paper›PMID 17085788›Full record

ReviewClinical reviews in allergy & immunology

Current issues with beta2-adrenoceptor agonists: pharmacology and molecular and cellular mechanisms.

Gary P Anderson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 5 pooled it
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 5 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Article
  8. Asthma and COPD: A Focus on β-Agonists - Past, Present and Future.Handbook of experimental pharmacology · 2024
    Review
  9. Article
  10. βLung · 2021
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Tiotropium in asthma: what is the evidence and how does it fit in?The World Allergy Organization journal · 2016
    Review
  16. Article
  17. Article
  18. An environmental epigenetic study of ADRB2 5'-UTR methylation and childhood asthma severity.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2012
    Article
  19. Article
  20. Albuterol modulates its own transepithelial flux via changes in paracellular permeability.American journal of respiratory cell and molecular biology · 2012
    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

1 author at 1 institution in 1 country.

Gary P AndersonLung Disease Research Group, Cooperative Research Centre for Chronic Inflammatory Diseases, Departments of Medicine and Pharmacology, The University of Melbourne, Parkville, Australia. gpa@unimelb.edu.au <gpa@unimelb.edu.au>
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beta2-adrenoceptors are widely, almost ubiquitously, expressed. Activation of these receptors on bronchial smooth muscle by short- and long-acting beta2-adrenoceptor agonists causes bronchodilation. Here, the beta2-adrenoceptor is linked by the G protein, Gs, to adenylyl cyclase, which increases cyclic adenosine monophosphate (cAMP), thus activating protein kinase A, which affects calcium levels and reduces the efficiency of myosin light-chain kinase, causing relaxation. Activation also entrains numerous acute and longer term downregulation responses affecting the number, location, and net efficiency of signaling of the receptor. Synthetic beta2-agonists are all "partial agonists," incompletely able to optimally stimulate cAMP signal transduction. However, compared with some cells (such as mast cells) involved in exercise- induced asthma induction, airway smooth muscle is privileged in that transduction efficiency is intrinsically high and the tissue is very resistant to complete downregulation. Glucocorticosteroids have broadly beneficial interactions with beta2-adrenoceptors. Researchers have recently discovered that the beta2-adrenoceptor may function as a homodimer and that it can form heterodimers with both the beta1- and beta3-adrenoceptors, and possibly other receptors. This further complicates interpretation of the effect of beta2-adrenoceptor polymorphisms, but it is unknown whether this occurs in humans in vivo. Researchers have known for some time that strong contraction involving receptors coupled to the Gq G protein (e.g., cholinergic and leukotriene receptors via negative biochemical crosstalk), virus infection (via uncoupling), and inflammation (via kinases) can impair relaxation. Most recently, researchers have discovered that the beta2-adrenoceptor can also send potentially adverse signals after "atypical coupling" to Gq rather than Gs. The clinical implications of these uncouplings, crosstalk, and atypical coupling possibilities are not well-understood.

Indexed as

Adrenergic beta-2 Receptor AgonistsAdrenergic beta-AgonistsBronchodilator AgentsHumansSignal TransductionAdrenergic beta-2 Receptor AgonistsAdrenergic beta-AgonistsBronchodilator Agents

Identifiers

PMID17085788
OpenAlexW2333257981

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.