Evidence map›Paper›PMID 23266596›Full record

ReviewJournal of molecular and cellular cardiology2013

CaV1.2 signaling complexes in the heart.

Robert D Harvey, Johannes W Hell

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. CACNA1C-Related Channelopathies.Handbook of experimental pharmacology · 2023
    Review
  16. Article
  17. Sympathetic Nervous System Regulation of Cardiac Calcium Channels.Handbook of experimental pharmacology · 2023
    Article
  18. Review
  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

2 authors.

Robert D HarveyDepartment of Pharmacology, University of Nevada School of Medicine, Reno, NV 89557, USA. rdharvey@unr.edu
Johannes W Hell

Funding

Predoctoral Training in the Pharmacological SciencesT32GM067795 · NIGMS · UNIVERSITY OF IOWA · PI STRACK, STEFAN · 2004 to 2021
$3.4M
POSTSYNAPTIC SIGNALING PATHWAYSR01NS035563 · NINDS · UNIVERSITY OF WISCONSIN MADISON · PI HELL, JOHANNES W · 1997 to 2010
$3.1M
Signaling by cAMP within postsynaptic nano domains R01NS078792R01NS078792 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HELL, JOHANNES W · 2012 to 2016
$2.0M
Mechanisms of cAMP CompartmentationR01GM101928 · NIGMS · UNIVERSITY OF NEVADA RENO · PI HARVEY, ROBERT D · 2012 to 2015
$1.1M
NIGMS NIH HHS R01 GM101928NIGMS NIH HHS T32 GM067795NINDS NIH HHS R01 NS035563NINDS NIH HHS R01 NS078792
6 · The paper itself

Abstract

L-type Ca(2+) channels (LTCCs) are essential for generation of the electrical and mechanical properties of cardiac muscle. Furthermore, regulation of LTCC activity plays a central role in mediating the effects of sympathetic stimulation on the heart. The primary mechanism responsible for this regulation involves β-adrenergic receptor (βAR) stimulation of cAMP production and subsequent activation of protein kinase A (PKA). Although it is well established that PKA-dependent phosphorylation regulates LTCC function, there is still much we do not understand. However, it has recently become clear that the interaction of the various signaling proteins involved is not left to completely stochastic events due to random diffusion. The primary LTCC expressed in cardiac muscle, CaV1.2, forms a supramolecular signaling complex that includes the β2AR, G proteins, adenylyl cyclases, phosphodiesterases, PKA, and protein phosphatases. In some cases, the protein interactions with CaV1.2 appear to be direct, in other cases they involve scaffolding proteins such as A kinase anchoring proteins and caveolin-3. Functional evidence also suggests that the targeting of these signaling proteins to specific membrane domains plays a critical role in maintaining the fidelity of receptor mediated LTCC regulation. This information helps explain the phenomenon of compartmentation, whereby different receptors, all linked to the production of a common diffusible second messenger, can vary in their ability to regulate LTCC activity. The purpose of this review is to examine our current understanding of the signaling complexes involved in cardiac LTCC regulation.

Indexed as

Calcium SignalingA Kinase Anchor ProteinsCalciumCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesHumansMyocardiumMyocytes, CardiacReceptors, Adrenergic, betaReceptors, Prostaglandin EA Kinase Anchor ProteinsCalciumCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesL-type calcium channel alpha(1C)Receptors, Adrenergic, betaReceptors, Prostaglandin E

Identifiers

PMID23266596
PMCPMC3628296

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Registered trials

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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.