Evidence map›Paper›PMID 24994983›Full record

ReviewFrontiers in pharmacology2014

Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.

Kevin P Vincent, Andrew D McCulloch, Andrew G Edwards

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. L-type CaPhysiological reports · 2022
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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 at 2 institutions in 2 countries.

Kevin P VincentDepartment of Bioengineering, University of California San Diego La Jolla, CA, USA.
Andrew D McCullochDepartment of Bioengineering, University of California San Diego La Jolla, CA, USA ; Department of Medicine, University of California San Diego La Jolla, CA, USA.
Andrew G EdwardsDepartment of Bioengineering, University of California San Diego La Jolla, CA, USA ; Institute for Experimental Medicine, Oslo University Hospital Ullevål Oslo, Norway ; Simula Research Laboratory Lysaker, Norway.
La Jolla Bioengineering Institute · USUniversity of California, San Diego · US

Funding

National Biomedical Computation Resource - Competitive Revision SupplementP41GM103426 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AMARO, ROMMIE E · 2012 to 2019
$14.0M
The Virtual Physiological Rat ProjectP50GM094503 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2011 to 2015
$11.6M
Training in Multi-Scale Analysis of Biological Structure and FunctionT32EB009380 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Andrew D. McCulloch, Padmini Rangamani · 2009 to 2026
$4.8M
Integrative Bioengineering of Heart, Vessels, and BloodT32HL105373 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, INTAGLIETTA, MARCOS · 2010 to 2019
$3.6M
Multi-scale Systems Model of Murine Heart FailureR01HL105242 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERS, DONALD M, MCCULLOCH, ANDREW D. · 2012 to 2016
$3.5M
Multi-Scale Modeling of the Failing Heart for Cardiac Rysynchronization TherapyR01HL096544 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D. · 2009 to 2013
$1.8M
NHLBI NIH HHS R01 HL096544NHLBI NIH HHS R01 HL105242NHLBI NIH HHS T32 HL105373NIBIB NIH HHS T32 EB009380NIGMS NIH HHS P41 GM103426NIGMS NIH HHS P50 GM094503
6 · The paper itself

Abstract

Calcium/calmodulin-dependent protein kinase II (CaMKII) activity has been shown to contribute to arrhythmogenesis in a remarkably broad range of cardiac pathologies. Several of these involve significant structural and electrophysiologic remodeling, whereas others are due to specific channelopathies, and are not typically associated with arrhythmogenic changes to protein expression or cellular and tissue structure. The ability of CaMKII to contribute to arrhythmia across such a broad range of phenotypes suggests one of two interpretations regarding the role of CaMKII in cardiac arrhythmia: (1) some CaMKII-dependent mechanism is a common driver of arrhythmia irrespective of the specific etiology of the disease, or (2) these different etiologies expose different mechanisms by which CaMKII is capable of promoting arrhythmia. In this review, we dissect the available mechanistic evidence to explore these two possibilities and discuss how the various molecular actions of CaMKII promote arrhythmia in different pathophysiologic contexts.

Indexed as

afterdepolarizationsarrhythmiasCaMKIIcardiovascular diseasesryanodine receptor

Identifiers

PMID24994983
PMCPMC4062880
OpenAlexW2068401800

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.