Evidence map›Paper›PMID 28170359›Full record

ReviewJournal of cardiovascular pharmacology2017

Targeting β3-Adrenergic Receptors in the Heart: Selective Agonism and β-Blockade.

Alessandro Cannavo, Walter J Koch

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2017. 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
3.7field-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

48 citing papers in PubMed, 88 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Current Perspectives of Mitochondria in Sepsis-Induced Cardiomyopathy.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. The βAdvances in pharmacological and pharmaceutical sciences · 2024
    Review
  11. Article
  12. Article
  13. Status of βReviews in cardiovascular medicine · 2023
    Review
  14. Compartmentalized cAMP signalling and control of cardiac rhythm.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  15. Review
  16. Article
  17. Article
  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.

Alessandro CannavoDepartment of Pharmacology, Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA.
Walter J Koch
Temple University · US

Funding

Targeting GRK2 in the HeartR01HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 1998 to 2022
$4.2M
Targeting GRK2 (BARK1) in Heart FailureR37HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2009 to 2018
$3.9M
NHLBI NIH HHS R01 HL061690NHLBI NIH HHS R37 HL061690
6 · The paper itself

Abstract

Cardiac diseases, such as heart failure, remain leading causes of morbidity and mortality worldwide, with myocardial infarction as the most common etiology. HF is characterized by β-adrenergic receptor (βAR) dysregulation that is primarily due to the upregulation of G protein-coupled receptor kinases that leads to overdesensitization of β1 and β2ARs, and this clinically manifests as a loss of inotropic reserve. Interestingly, the "minor" βAR isoform, the β3AR, found in the heart, lacks G protein-coupled receptor kinases recognition sites, and is not subject to desensitization, and as a consequence of this, in human failing myocardium, the levels of this receptor remain unchanged or are even increased. In different preclinical studies, it has been shown that β3ARs can activate different signaling pathways that can protect the heart. The clinical relevance of this is also supported by the effects of β-blockers which are well known for their proangiogenic and cardioprotective effects, and data are emerging showing that these are mediated, at least in part, by enhancement of β3AR activity. In this regard, targeting of β3ARs could represent a novel potential strategy to improve cardiac metabolism, function, and remodeling.

Indexed as

Adrenergic beta-3 Receptor AgonistsAdrenergic beta-3 Receptor AntagonistsAnimalsDrug Delivery SystemsHeartHeart DiseasesHumansReceptors, Adrenergic, beta-3Adrenergic beta-3 Receptor AgonistsAdrenergic beta-3 Receptor AntagonistsReceptors, Adrenergic, beta-3

Identifiers

PMID28170359
PMCPMC5295490
OpenAlexW2550433123

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.