Evidence map›Paper›PMID 19719781›Full record

ReviewBritish journal of pharmacology2009

Stimulation of cardiac beta-adrenoceptors targets connexin 43.

Kerstin Boengler

Open access · bronzeAbstract readCommentReview
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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. GPCR theme editorial.British journal of pharmacology · 2009
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kerstin BoenglerInstitut für Pathophysiologie, Universitätsklinikum Essen, Germany. Kerstin.boengler@uk-essen.de
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Connexin 43 (Cx43) is the major protein of cardiac ventricular gap junctions and is crucial to cell-cell communication and cardiac function. The protein level of Cx43 is reduced in patients with heart failure or dilated cardiomyopathy (DCM), pathophysiological conditions often associated with arrhythmias. As catecholamines are often increased in cardiac diseases, Salameh et al., in this issue of the BJP, investigated the effect of beta-adrenoceptor stimulation of neonatal cardiomyocytes on Cx43 expression and found increased Cx43 mRNA and protein levels following 24 h stimulation. Up-regulation of Cx43 was associated with phosphorylation of mitogen-activated protein kinases and translocation of transcription factors into the nucleus. In patients with DCM, a situation often associated with desensitization of the beta-adrenoceptor system, Cx43 expression was reduced. The characterization of the signal transduction pathways involved in Cx43 expression and intracellular localization in human myocardium in vivo is a promising target for the development of new anti-arrhythmic strategies.

Indexed as

Drug Delivery SystemsAnimalsCardiovascular AgentsConnexin 43HumansMyocardiumReceptors, Adrenergic, betaCardiovascular AgentsConnexin 43Receptors, Adrenergic, beta

Identifiers

PMID19719781
PMCPMC2795258
OpenAlexW2080630852

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.