Evidence map›Paper›PMID 32844365›Full record

ArticleJournal of cardiovascular translational research2021

Activation of AMP-Activated Protein Kinases Prevents Atrial Fibrillation.

Cevher Ozcan, Gunjan Dixit, Zhenping Li

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 2021. 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
1.1field-weighted citation impact, top 18% 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, 25 citations in OpenAlex.

  1. Article
  2. Metformin Protects Against Persistent Atrial Fibrillation in an Equine Model.Circulation. Arrhythmia and electrophysiology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Mouse models of spontaneous atrial fibrillation.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Implications of SGLT Inhibition on Redox Signalling in Atrial Fibrillation.International journal of molecular sciences · 2021
    Review
  18. 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

3 authors at 1 institution in 1 country.

Cevher OzcanDepartment of Medicine, Section of Cardiology, Heart and Vascular Center, University of Chicago Medical Center, Chicago, IL, USA. cozcan@uchicago.edu.
Gunjan DixitDepartment of Medicine, Section of Cardiology, Heart and Vascular Center, University of Chicago Medical Center, Chicago, IL, USA.
Zhenping LiDepartment of Medicine, Section of Cardiology, Heart and Vascular Center, University of Chicago Medical Center, Chicago, IL, USA.
University of Chicago Medical Center · US

Funding

Mitochondrial Mechanisms and Novel Therapeutic Targets in Atrial FibrillationK08HL117082 · NHLBI · UNIVERSITY OF CHICAGO · PI OZCAN, CEVHER · 2014 to 2018
$798k
NHLBI NIH HHS K08 HL117082NHLBI NIH HHS K08HL117082
6 · The paper itself

Abstract

Atrial fibrillation (AF) is common, yet there is no preventive therapy for AF. We tested the efficacy of AMP-activated protein kinase (AMPK) activators, metformin, and aspirin, in primary prevention of AF in cardiac-specific liver kinase B1 (LKB1) knockout (KO) mouse model of AF. Incidence of spontaneous AF was significantly reduced in treated KO mice with metformin (10 mg/kg/day) (8.3% in male and 10.3% in female) and aspirin (20 mg/kg/day) (29.4% in male and 21.4% in female) compared with untreated littermates (81% in male and 67% in female) at 8 weeks (p < 0.05). Prevention of AF was associated with activation of AMPK in treated mice and thereby improvement of mitochondrial function, gap junction proteins (connexin 40/43), and intra- and inter-cellular ultrastructure in atrial myocardium. Fibrosis was significantly less in treated mice atria. Pharmacological activation of AMPK is an effective upstream therapy for the primary prevention of AF in susceptible heart. Graphical abstract.

Indexed as

AMP-Activated Protein KinasesAnimalsAnti-Arrhythmia AgentsAspirinAtrial FibrillationAtrial RemodelingDisease Models, AnimalEnzyme ActivationEnzyme ActivatorsFemaleFibrosisHeart RateMaleMetforminMiceMice, Inbred C57BLAMP-Activated Protein KinasesAnti-Arrhythmia AgentsAspirinEnzyme ActivatorsMetforminStk11 protein, mouseAMPKAspirinAtrial fibrillationMetforminPharmacotherapyTherapeutic intervention

Identifiers

PMID32844365
OpenAlexW3081495736

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.