Evidence map›Paper›PMID 25577293›Full record

ReviewTrends in cardiovascular medicine2015

Role of CaMKII in cardiac arrhythmias.

Thomas J Hund, Peter J Mohler

Abstract readReview
In one paragraph

Review in Trends in cardiovascular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Potential Roles of IPBiomolecules · 2024
    Review
  6. Review
  7. Article
  8. Changes in cellular CaThe Journal of physiology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Thomas J HundThe Dorothy M. Davis Heart & Lung Research Institute, OH; Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH; Department of Biomedical Engineering, The Ohio State University College of Engineering, Columbus, OH.
Peter J MohlerThe Dorothy M. Davis Heart & Lung Research Institute, OH; Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH; Department of Physiology & Cell Biology, The Ohio State University Wexner Medical Center, Columbus, OH. Electronic address: peter.mohler@osumc.edu.
The Ohio State University Wexner Medical Center · US

Funding

Role of spectrin/ankyrin-G complex in myocyte signaling and cardiac excitabilityR01HL083422 · NHLBI · VANDERBILT UNIVERSITY · PI MOHLER, PETER J. · 2006 to 2016
$3.8M
Role of ankyrin-B in human arrhythmiaR01HL084583 · NHLBI · UNIVERSITY OF IOWA · PI MOHLER, PETER J. · 2006 to 2015
$3.4M
Training in Congenital and Acquired Heart DiseaseT32HL098039 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU, MOHLER, PETER J. · 2009 to 2019
$2.5M
EHD proteins in cardiac membrane protein targeting and remodelingR01HL114383 · NHLBI · OHIO STATE UNIVERSITY · PI BOYDEN, PENELOPE ALTMAN, MOHLER, PETER J. · 2013 to 2016
$2.1M
CaMKII-dependent regulation of cardiac excitabilityR01HL114893 · NHLBI · OHIO STATE UNIVERSITY · PI HUND, THOMAS JEFFREY · 2012 to 2016
$1.9M
NHLBI NIH HHS HL083422NHLBI NIH HHS HL084583NHLBI NIH HHS HL114383NHLBI NIH HHS HL114893NHLBI NIH HHS R01 HL083422NHLBI NIH HHS R01 HL084583NHLBI NIH HHS R01 HL114383NHLBI NIH HHS R01 HL114893NHLBI NIH HHS T32 HL098039
6 · The paper itself

Abstract

Protein phosphorylation is a central mechanism in vertebrates for the regulation of signaling. With regard to the cardiovascular system, phosphorylation of myocyte targets is critical for the regulation of excitation contraction coupling, metabolism, intracellular calcium regulation, mitochondrial activity, transcriptional regulation, and cytoskeletal dynamics. In fact, pathways that tune protein kinase signaling have been a mainstay for cardiovascular therapies for the past 60 years. The calcium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine kinase with numerous roles in human physiology. Dysfunction in CaMKII-based signaling has been linked with a host of cardiovascular phenotypes including heart failure and arrhythmia, and CaMKII levels are elevated in human and animal disease models of heart disease. While nearly a decade has been invested in targeting CaMKII for the treatment of heart failure and arrhythmia phenotypes, to date, approaches to target the molecule for antiarrhythmic benefit have been unsuccessful for reasons that are still not entirely clear, although (1) lack of compound specificity and (2) the multitude of downstream targets are likely contributing factors. This review will provide an update on current pathways regulated by CaMKII with the goal of illustrating potential upstream regulatory mechanisms and downstream targets that may be modulated for the prevention of cardiac electrical defects. While the review will cover multiple aspects of CaMKII dysfunction in cardiovascular disease, we have given special attention to the potential of CaMKII-associated late Na(+) current as a novel therapeutic target for cardiac arrhythmia.

Indexed as

Arrhythmias, CardiacCalcium-Calmodulin-Dependent Protein Kinase Type 2HumansModels, TheoreticalMolecular Targeted TherapySignal TransductionCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID25577293
PMCPMC4458226
OpenAlexW2099587689

What OpenQuestion holds

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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.