Evidence map›Paper›PMID 33035439›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2020

Inhibition of cardiac potassium currents by oxidation-activated protein kinase A contributes to early afterdepolarizations in the heart.

M Trum, M M T Islam, S Lebek, M Baier, P Hegner, P Eaton, L S Maier, S Wagner

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  9. Review
  10. Article
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  12. Article
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  14. Enhanced Heart Failure in Redox-Dead Cys17Ser PKARIα Knock-In Mice.Journal of the American Heart Association · 2021
    Article
  15. Review
  16. Review
  17. Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to NaInternational journal of molecular sciences · 2021
    Review
  18. Regulation of Cardiac PKA Signaling by cAMP and Oxidants.Antioxidants (Basel, Switzerland) · 2021
    Review
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

8 authors at 3 institutions in 3 countries.

M TrumDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0002-8267-2681
M M T IslamDepartment of Biochemistry and Molecular Biology, University of Dhaka, Bangladesh.
S LebekDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
M BaierDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
P HegnerDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
P EatonThe William Harvey Research Institute, Charterhouse Square, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
L S MaierDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
S WagnerDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
University Hospital Regensburg · DEQueen Mary University of London · GBUniversity of Dhaka · BD

Funding

British Heart Foundation PG/19/33/34385British Heart Foundation RG/17/16/33294Medical Research Council G0700320Medical Research Council MR/P023150/1Medical Research Council MR/P023150/2Medical Research Council MR/R01065X/1Medical Research Council MR/R01065X/2
6 · The paper itself

Abstract

Reactive oxygen species (ROS) have been shown to prolong cardiac action potential duration resulting in afterdepolarizations, the cellular basis of triggered arrhythmias. As previously shown, protein kinase A type I (PKA I) is readily activated by oxidation of its regulatory subunits. However, the relevance of this mechanism of activation for cardiac pathophysiology is still elusive. In this study, we investigated the effects of oxidation-activated PKA I on cardiac electrophysiology. Ventricular cardiomyocytes were isolated from redox-dead PKA-RI Cys17Ser knock-in (KI) and wild-type (WT) mice and exposed to H

Indexed as

Action PotentialsHeart RateAnimalsCyclic AMP-Dependent Protein Kinase RIalpha SubunitEnzyme ActivationHydrogen PeroxideMaleMice, Inbred C57BLMice, TransgenicMutationMyocytes, CardiacOxidation-ReductionOxidative StressPotassiumPotassium ChannelsProtein MultimerizationCyclic AMP-Dependent Protein Kinase RIalpha SubunitHydrogen PeroxidePotassiumPotassium ChannelsPrkar1a protein, mousearrhythmiaearly afterdepolarizationoxidative stresspotassium currentsprotein kinase A

Identifiers

PMID33035439
PMCPMC7792712
OpenAlexW3091930065

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.