Evidence map›Paper›PMID 23345264›Full record

ReviewCardiovascular research2013

Spatial control of the βAR system in heart failure: the transverse tubule and beyond.

Julia Gorelik, Peter T Wright, Alexander R Lyon, Sian E Harding

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 53 citations in OpenAlex.

  1. Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026
    Review
  2. Article
  3. Article
  4. Changes in cellular CaThe Journal of physiology · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. CaCold Spring Harbor perspectives in biology · 2020
    Review
  12. Review
  13. Review
  14. The role of spatial organization of CaBasic research in cardiology · 2017
    Article
  15. Review
  16. Review
  17. Cardiac T-Tubule Microanatomy and Function.Physiological reviews · 2017
    Review
  18. Article
  19. Review
  20. Review
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

4 authors at 2 institutions in 2 countries.

Julia GorelikDepartment of Cardiovascular Medicine, National Heart and Lung Institute, Imperial College, 4th floor, Imperial Centre for Translational and Experimental Medicine, Hammersmith Campus, Du Cane Road, London W12 0NN, UK. j.gorelik@ic.ac.uk
Peter T Wright
Alexander R Lyon
Sian E Harding
Hammersmith Hospital · GBRoyal Brompton Hospital · GB

Funding

British Heart Foundation FS/11/67/28954British Heart Foundation NH/10/3/28574British Heart Foundation RG/12/18/30088Medical Research Council G0500373Wellcome Trust WTN090594
6 · The paper itself

Abstract

The beta1-adrenoceptors (β(1)AR) and beta-2 (β(2)AR) adrenoceptors represent the predominant pathway for sympathetic control of myocardial function. Diverse mechanisms have evolved to translate signalling via these two molecules into differential effects on physiology. In this review, we discuss how the functions of the βAR are organized from the level of secondary messengers to the whole heart to achieve this. Using novel microscopy and bio-imaging methods researchers have uncovered subtle organization of the control of cyclic adenosine monophosphate (cAMP), the predominant positively inotropic pathway for the βAR. The β(2)AR in particular is demonstrated to give rise to highly compartmentalized, spatially confined cAMP signals. Organization of β(2)AR within the T-tubule and caveolae of cardiomyocytes concentrates this receptor with molecules which buffer and shape its cAMP signal to give fine control. This situation is undermined in various forms of heart failure. Human and animal models of heart failure demonstrate disruption of cellular micro-architecture which contributes to the change in response to cardiac βARs. Loss of cellular structure has proved key to the observed loss of confined β(2)AR signalling. Some pharmacological and genetic treatments have been successful in returning failing cells to a more structured phenotype. Within these cells it has been possible to observe the partial restoration of normal β(2)AR signalling. At the level of the organ, the expression of the two βAR subtypes varies between regions with the β(2)AR forming a greater proportion of the βAR population at the apex. This distribution may contribute to regional wall motion abnormalities in Takotsubo cardiomyopathy, a syndrome of high sympathetic activity, where the phosphorylated β(2)AR can signal via Gi protein to produce negatively inotropic effects.

Indexed as

Amino Acid Transport System y+LAnimalsCaveolaeCyclic AMPCyclic AMP-Dependent Protein KinasesDisease Models, AnimalHeart FailureHumansMyocardial ContractionMyocytes, CardiacNeoplasm ProteinsReceptors, Adrenergic, betaSarcoplasmic ReticulumSignal TransductionAmino Acid Transport System y+LCyclic AMPCyclic AMP-Dependent Protein KinasesNeoplasm ProteinsReceptors, Adrenergic, betaSLC43A1 protein, human

Identifiers

PMID23345264
PMCPMC3633155
OpenAlexW2149857949

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.