Evidence map›Paper›PMID 32198206›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Loss of insulin signaling may contribute to atrial fibrillation and atrial electrical remodeling in type 1 diabetes.

Iuliia Polina, Hailey J Jansen, Tiesong Li, Motahareh Moghtadaei, Loryn J Bohne, Yingjie Liu, Pooja Krishnaswamy, Emmanuel E Egom, Darrell D Belke, Sara A Rafferty and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
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  4. Metabolic and Inflammatory Mechanisms Driving Atrial Fibrillation.Annual review of pharmacology and toxicology · 2026
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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

13 authors at 3 institutions in 1 country.

Iuliia PolinaDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Hailey J JansenDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Tiesong LiDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Motahareh MoghtadaeiDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Loryn J BohneLibin Cardiovascular Institute of Alberta, Department of Cardiac Sciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada, T2N 4Z6.
Yingjie LiuLibin Cardiovascular Institute of Alberta, Department of Cardiac Sciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada, T2N 4Z6.
Pooja KrishnaswamyDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Emmanuel E EgomDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Darrell D BelkeLibin Cardiovascular Institute of Alberta, Department of Cardiac Sciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada, T2N 4Z6.
Sara A RaffertyDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Martin EzeaniDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2.
Anne M GillisLibin Cardiovascular Institute of Alberta, Department of Cardiac Sciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada, T2N 4Z6.
Robert A RoseDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, NS, Canada, B3H 4R2; robert.rose@ucalgary.ca.
Dalhousie University · CALibin Cardiovascular Institute of Alberta · CAUniversity of Calgary · CA

Funding

CIHR MOP 142486CIHR PJT 166105
6 · The paper itself

Abstract

Atrial fibrillation (AF) is prevalent in diabetes mellitus (DM); however, the basis for this is unknown. This study investigated AF susceptibility and atrial electrophysiology in type 1 diabetic Akita mice using in vivo intracardiac electrophysiology, high-resolution optical mapping in atrial preparations, and patch clamping in isolated atrial myocytes. qPCR and western blotting were used to assess ion channel expression. Akita mice were highly susceptible to AF in association with increased P-wave duration and slowed atrial conduction velocity. In a second model of type 1 DM, mice treated with streptozotocin (STZ) showed a similar increase in susceptibility to AF. Chronic insulin treatment reduced susceptibility and duration of AF and shortened P-wave duration in Akita mice. Atrial action potential (AP) morphology was altered in Akita mice due to a reduction in upstroke velocity and increases in AP duration. In Akita mice, atrial Na

Indexed as

Action PotentialsAnimalsAtrial FibrillationAtrial RemodelingCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease Models, AnimalEchocardiographyElectrocardiographyHeart AtriaHumansInsulinKv1.5 Potassium ChannelMaleMiceIns2 protein, mouseInsulinKv1.5 Potassium ChannelNAV1.5 Voltage-Gated Sodium ChannelPotassiumSodiumStreptozocinaction potentialatrial fibrillationdiabetes mellitusNa+ currentphosphoinositide 3-kinase

Identifiers

PMID32198206
PMCPMC7148583
OpenAlexW3011256017

What Socratic 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 Socratic graph.