Evidence map›Paper›PMID 34217833›Full record

ReviewCellular signalling2021

Serine-threonine protein phosphatase regulation of Cx43 dephosphorylation in arrhythmogenic disorders.

Xun Ai, Jiajie Yan, Steven M Pogwizd

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. 2-Aminoethoxydiphenyl borate induces arrhythmias via Cx43-S282 dephosphorylation.In vitro cellular & developmental biology. Animal · 2026
    Article
  2. Genetic loci responsible for atrioventricular block in children.Frontiers in cell and developmental biology · 2026
    Review
  3. Article
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  8. Saturated fatty acids stimulate cytokine production in tanycytes via the PP2Ac-dependent signaling pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  9. Review
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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 1 country.

Xun AiDepartment of Physiology & Biophysics, Rush University, Chicago, IL, United States of America.
Jiajie YanDepartment of Physiology & Biophysics, Rush University, Chicago, IL, United States of America.
Steven M PogwizdDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America. Electronic address: spogwizd@uab.edu.
Rush University · USUniversity of Alabama at Birmingham · US

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
The Stress Response Kinase JNK and Alcohol Evoked Atrial FibrillationR01AA024769 · NIAAA · OHIO STATE UNIVERSITY · PI AI, XUN · 2017 to 2021
$3.3M
Heart-platelet crosstalk: JNK, AF, and thrombogenesisR01HL146744 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI Xun Ai, Yuchi Han · 2019 to 2026
$3.2M
Atrial and blood JNK in Postoperative AFR01HL168728 · NHLBI · OHIO STATE UNIVERSITY · PI Xun Ai · 2023 to 2026
$2.7M
JNK Suppression of Connexin43 Enhances Atrial Fibrillation in Aged AtriaR01HL113640 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AI, XUN · 2012 to 2015
$1.5M
NHLBI NIH HHS P01 HL080101NHLBI NIH HHS R01 HL113640NHLBI NIH HHS R01 HL146744NHLBI NIH HHS R01 HL168728NIAAA NIH HHS R01 AA024769
6 · The paper itself

Abstract

Regulation of cell-to-cell communication in the heart by the gap junction protein Connexin43 (Cx43) involves modulation of Cx43 phosphorylation state by protein kinases, and dephosphorylation by protein phosphatases. Dephosphorylation of Cx43 has been associated with impaired intercellular coupling and enhanced arrhythmogenesis in various pathologic states. While there has been extensive study of the protein kinases acting on Cx43, there has been limited studies of the protein phosphatases that may underlie Cx43 dephosphorylation. The focus of this review is to introduce serine-threonine protein phosphatase regulation of Cx43 phosphorylation state and cell-to-cell communication, and its impact on arrhythmogenesis in the setting of chronic heart failure and myocardial ischemia, as well as on atrial fibrillation. We also discuss the therapeutic potential of modulating protein phosphatases to treat arrhythmias in these clinical settings.

Indexed as

Connexin 43Gap JunctionsCell CommunicationPhosphoprotein PhosphatasesPhosphorylationSerineThreonineConnexin 43Phosphoprotein PhosphatasesSerineThreonineCalcineurinConnexin 43DephosphorylationPP1PP2AProtein phosphatase

Identifiers

PMID34217833
PMCPMC8963383
OpenAlexW3181719290

What Socratic 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 Socratic graph.