Evidence map›Paper›PMID 17874127›Full record

ReviewPflugers Archiv : European journal of physiology2008

Genetically changed mice with chronic deficiency or overexpression of the beta-adrenoceptors--what can we learn for the therapy of heart failure?

Samuel Lee, Robert H G Schwinger, Klara Brixius

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Asthma and COPD: A Focus on β-Agonists - Past, Present and Future.Handbook of experimental pharmacology · 2024
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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.

Samuel LeeLaboratory of Muscle Research and Molecular Cardiology, Department III for Internal Medicine, University of Cologne, Cologne, Germany.
Robert H G Schwinger
Klara Brixius

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure is one of the most common medical diseases-almost every third 55-year-old person in the Western world is going to develop heart failure in his or her life. The development of heart failure is associated with pivotal restructuring of the beta-adrenergic system. The beta-adrenoceptor antagonists have emerged to be an essential part of the therapy of chronic heart failure. Three different beta-adrenoceptors could be identified and characterized so far. The beta1-adrenoceptors are being down-regulated, while the beta3-adrenoceptors are being up-regulated. The mechanisms that are responsible for the positive impact of beta-adrenoceptor antagonists are not completely understood up to now. Therefore, it is necessary to point out the crucial role of the beta-adrenergic system for the regulation of the cardiovascular system and the pathogenesis of heart failure. In the recent couple of years, numerous transgenic mouse models have proven to be helpful to gain a better understanding of the function and the relevance of these receptors. This review gives an overview of the pathophysiological relevance of the beta-adrenergic system for heart failure and outlines the most important insights concerning heart function, which could be derived from genetically changed mice with chronic deficiency and overexpression of the beta-adrenoceptor.

Indexed as

Disease Models, AnimalMice, KnockoutAnimalsChronic DiseaseHeart FailureHumansMiceReceptors, Adrenergic, betaReceptors, Adrenergic, beta

Identifiers

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.