Evidence map›Paper›PMID 28077320›Full record

ReviewJournal of molecular and cellular cardiology2017

Serine/Threonine Phosphatases in Atrial Fibrillation.

Jordi Heijman, Shokoufeh Ghezelbash, Xander H T Wehrens, Dobromir Dobrev

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  4. Targeted Metabolomic Biomarkers for Stroke Subtyping.Translational stroke research · 2024
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  5. The Dysfunction of CaInternational journal of molecular sciences · 2023
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  8. Review
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  11. Review
  12. Mechanisms of electrical remodeling in lipotoxic guinea pig heart.Biochemical and biophysical research communications · 2019
    Article
  13. Review
  14. Article
  15. Article
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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

4 authors at 3 institutions in 3 countries.

Jordi HeijmanDepartment of Cardiology, Cardiovascular Research Institute Maastricht, Faculty of Health, Medicine, and Life Sciences, Maastricht University, Maastricht, The Netherlands.
Shokoufeh GhezelbashInstitute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany.
Xander H T WehrensCardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Department of Medicine (Cardiology), Pediatrics, Baylor College of Medicine, Houston, USA.
Dobromir DobrevInstitute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany. Electronic address: dobromir.dobrev@uk-essen.de.
West German Heart and Vascular Center Essen · DEBaylor College of Medicine · USMaastricht University · NL

Funding

Ryanodine receptor regulation in post-operative atrial fibrillationR01HL089598 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2007 to 2022
$6.5M
Sex-specific arrhythmogenic mechanisms of atrial fibrillationR01HL131517 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Eleonora Grandi · 2016 to 2026
$5.0M
Regulation of Sarcoplasmic Reticulum Calcium Release in Heart FailureR01HL091947 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2009 to 2019
$3.2M
Determining the Role of Junctophilin-2 in Cardiac DiseaseR01HL117641 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2014 to 2017
$2.3M
Development of novel compounds for the treatment of atrial fibrillationR41HL129570 · NHLBI · ELEX BIOTECH, LLC · PI WEHRENS, XANDER H.T. · 2015 to 2015
$428k
NHLBI NIH HHS R01 HL089598NHLBI NIH HHS R01 HL091947NHLBI NIH HHS R01 HL117641NHLBI NIH HHS R01 HL131517NHLBI NIH HHS R41 HL129570
6 · The paper itself

Abstract

Serine/threonine protein phosphatases control dephosphorylation of numerous cardiac proteins, including a variety of ion channels and calcium-handling proteins, thereby providing precise post-translational regulation of cardiac electrophysiology and function. Accordingly, dysfunction of this regulation can contribute to the initiation, maintenance and progression of cardiac arrhythmias. Atrial fibrillation (AF) is the most common heart rhythm disorder and is characterized by electrical, autonomic, calcium-handling, contractile, and structural remodeling, which include, among other things, changes in the phosphorylation status of a wide range of proteins. Here, we review AF-associated alterations in the phosphorylation of atrial ion channels, calcium-handling and contractile proteins, and their role in AF-pathophysiology. We highlight the mechanisms controlling the phosphorylation of these proteins and focus on the role of altered dephosphorylation via local type-1, type-2A and type-2B phosphatases (PP1, PP2A, and PP2B, also known as calcineurin, respectively). Finally, we discuss the challenges for phosphatase research, potential therapeutic significance of altered phosphatase-mediated protein dephosphorylation in AF, as well as future directions.

Indexed as

Adenosine DiphosphateAnimalsAtrial FibrillationAtrial RemodelingCalciumCell CommunicationEnzyme ActivationGene ExpressionHumansMolecular Targeted TherapyMyocardial ContractionPhosphoprotein PhosphatasesAdenosine DiphosphateCalciumPhosphoprotein Phosphatasesatrial fibrillationcalcium handlingion channelsmyofilamentsprotein phosphatases

Identifiers

PMID28077320
PMCPMC5346472
OpenAlexW2568675678

What OpenQuestion holds

Textmetadata
LicenceTDM
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.