Evidence map›Paper›PMID 19422376›Full record

ReviewBritish journal of pharmacology2009

Beta 1- and beta 2-adrenoceptor polymorphisms and cardiovascular diseases.

Kirsten Leineweber, Gerd Heusch

Open access · bronzeAbstract readComparative StudyReview
In one paragraph

Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Association of polymorphisms in the beta-2 adrenergic receptor gene with fracture risk and bone mineral density.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2015
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. CRISPR/Cas9-mediated generation and analysis of N terminus polymorphic models of βMolecular therapy. Methods & clinical development · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Observational
  13. Genes and Cardiovascular Disease: Where do we go from here?Sultan Qaboos University medical journal · 2015
    Article
  14. Article
  15. Observational
  16. Article
  17. Review
  18. 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

2 authors at 1 institution in 1 country.

Kirsten LeineweberInstitute for Pathophysiology, University of Essen, School of Medicine, Essen, Germany. kirsten.leineweber@bayerhealthcare.com
Gerd Heusch
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beta(1)- and beta(2)-adrenoceptors (AR) play a pivotal role in the regulation of cardiovascular function. Both beta-AR subtypes are polymorphic: two single nucleotide polymorphisms (SNPs) have been described for the beta(1)- (Ser49Gly, Arg389Gly) and four for the beta(2)-AR (Arg-19Cys, Arg16Gly, Gln27Glu, Thr164Ile), and they are possibly of functional relevance. In recombinant cell systems, Gly49-beta(1)-AR are more susceptible to agonist-promoted down-regulation than Ser49-beta(1)-AR, whereas Arg389-beta(1)-AR are three to four times more responsive to agonist-evoked stimulation than Gly389-beta(1)-AR. With respect to beta(2)-AR, the Cys-19 variant is associated with greater beta(2)-AR expression than the Arg-19 variant; Gly16-beta(2)-AR are more susceptible, whereas Glu27-beta(2)-AR are almost resistant to agonist-promoted down-regulation; Thr164-beta(2)-AR are three to four times more responsive to agonist-evoked stimulation than Ile164-beta(2)-AR. Several studies addressed potential phenotypic consequences of these SNPs in vivo by influencing and/or contributing to the pathophysiology of cardiovascular/pulmonary diseases such as hypertension, congestive heart failure, arrhythmias or asthma. At present, it appears that these beta-AR SNPs are very likely not disease-causing genes but possibly predictive for the responsiveness to agonists and antagonists. Patients carrying one or two alleles of the Gly389-beta(1)-AR are poor or non-responders to agonists and antagonists, whereas patients homozygous for the Arg389-beta(1)-AR are good responders. Subjects carrying the Ile164-beta(2)-AR exhibit blunted responses to beta(2)-AR stimulation. Asthma patients carrying the Arg16-Gln27-Thr164-beta(2)-AR haplotype who receive regularly short- or long-acting beta(2)-AR agonists are rather susceptible to agonist-induced desensitization and in consequence exhibit reduced bronchodilating and -protective effects and/or increased asthma exacerbations. The clinical relevance of these findings is still under debate.

Indexed as

Adrenergic AgentsAnimalsCardiovascular DiseasesHumansPolymorphism, GeneticReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2Adrenergic AgentsReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2

Identifiers

PMID19422376
PMCPMC2795234
OpenAlexW1967214804

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.