Evidence map›Paper›PMID 26762270›Full record

ReviewCardiovascular research2016

Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal.

Olurotimi O Mesubi, Mark E Anderson

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Understanding the Diseased Atria.Physiology (Bethesda, Md.) · 2026
    Review
  3. Article
  4. Review
  5. Metabolic and Inflammatory Mechanisms Driving Atrial Fibrillation.Annual review of pharmacology and toxicology · 2026
    Review
  6. Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Dual effects of the small-conductance CaAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  17. Review
  18. CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023
    Review
  19. Review
  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 2 institutions in 1 country.

Olurotimi O MesubiDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Medicine, The Johns Hopkins University School of Medicine, 1830 E. Monument Street, Suite 9026, Baltimore, MD 21287, USA.
Mark E AndersonDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Medicine, The Johns Hopkins University School of Medicine, 1830 E. Monument Street, Suite 9026, Baltimore, MD 21287, USA Department of Physiology and the Program in Cellular and Molecular Medicine, The Johns Hopkins School of Medicine, Baltimore, MD, USA mark.anderson@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

PATHOPHYSIOLOGY OF MYOCARDIAL DISEASEST32HL007227 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Chulan Kwon, WENDY S POST · 1985 to 2026
$21.2M
Mitochondrial Calmodulin Kinase II in Physiology and DiseaseR01HL070250 · NHLBI · VANDERBILT UNIVERSITY · PI ANDERSON, MARK E · 2002 to 2017
$5.2M
Methionine sulfoxide reductase A and oxidized CaMKII in structural heart diseaseR01HL079031 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2006 to 2015
$3.3M
CaMKII in Sinus Node Physiology and DiseaseR01HL096652 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2009 to 2016
$3.0M
Oxidized CaMKII in Atrial FibrillationR01HL113001 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2012 to 2016
$1.9M
NHLBI NIH HHS R01-HL070250NHLBI NIH HHS R01-HL079031NHLBI NIH HHS R01-HL096652NHLBI NIH HHS R01-HL113001NHLBI NIH HHS T32 HL007227NHLBI NIH HHS T32-HL007227
6 · The paper itself

Abstract

CaMKII is a serine-threonine protein kinase that is abundant in myocardium. Emergent evidence suggests that CaMKII may play an important role in promoting atrial fibrillation (AF) by targeting a diverse array of proteins involved in membrane excitability, cell survival, calcium homeostasis, matrix remodelling, inflammation, and metabolism. Furthermore, CaMKII inhibition appears to protect against AF in animal models and correct proarrhythmic, defective intracellular Ca(2+) homeostasis in fibrillating human atrial cells. This review considers current concepts and evidence from animal and human studies on the role of CaMKII in AF.

Indexed as

AnimalsAtrial FibrillationAtrial RemodelingCalcium-Calmodulin-Dependent Protein Kinase Type 2Heart AtriaHeart Conduction SystemHumansMyocardiumCalcium-Calmodulin-Dependent Protein Kinase Type 2ArrhythmiasAtrial fibrillationAtrial remodellingCaMKII

Identifiers

PMID26762270
PMCPMC4777912
OpenAlexW2255607281

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.