Evidence map›Paper›PMID 32855719›Full record

ArticleExperimental and therapeutic medicine2020

Exendin-4 inhibits atrial arrhythmogenesis in a model of myocardial infarction-induced heart failure via the GLP-1 receptor signaling pathway.

Jingjing Chen, Shunen Xu, Long Wang, Wei Zhou, Ping Li, Na Deng, Qian Tang, Yongkang Li, Lirong Wu, Jiulin Chen and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Observational
  5. Review
  6. Review
  7. Article
  8. 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

11 authors at 2 institutions in 1 country.

Jingjing ChenDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Shunen XuDepartment of Orthopedic Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Long WangDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Wei ZhouDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Ping LiDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Na DengDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Qian TangDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Yongkang LiDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Lirong WuDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Jiulin ChenDepartment of Cardiology, Qian Xi Nan People's Hospital, Bijie, Guizhou 562400, P.R. China.
Wei LiDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Affiliated Hospital of Guizhou Medical University · CNGuiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon-like peptide-1 receptor (GLP-1 receptor) agonists are considered to exert cardioprotective effects in models of acute and chronic heart disease. The present study aimed to investigate the role of exendin-4 (a GLP-1 receptor agonist) in atrial arrhythmogenesis in a model of myocardial infarction (MI)-induced heart failure and to elucidate the mechanisms underlying its effects. For this purpose, male Sprague-Dawley rats underwent sham surgery or left anterior descending artery ligation prior to being treated with saline/exendin-4/exendin-4 plus exendin9-39 (an antagonist of GLP-1 receptor) for 4 weeks. The effects of exendin-4 on atrial electrophysiology, atrial fibrosis and PI3K/AKT signaling were assessed. Rats with MI exhibited depressed left ventricular function, an enlarged left atrium volume, prolonged action potential duration, elevated atrial tachyarrhythmia inducibility, decreased conduction velocity and an increased total activation time, as well as total activation time dispersion and atrial fibrosis. However, these abnormalities were attenuated by treatment with the GLP-1 receptor agonist, exendin-4. Moreover, the expression levels of collagen I, collagen III, transforming growth factor-β1, phosphorylated PI3K and AKT levels in atrial tissues were upregulated in rats with MI. These changes were also attenuated by exendin-4. It was also found that these exedin-4-mediated attenutations were mitigated by the co-administration of exendin9-39 with exendin-4. Overall, the findings of the present study suggested that exendin-4 decreases susceptibility to atrial arrhythmogenesis, improves conduction properties and exerts antifibrotic effects via the GLP-1 receptor signaling pathway. These findings provide evidence for the potential use of GLP-1R in the treatment of atrial fibrillation.

Indexed as

cardiac electrophysiologyfibrosisheart failure

Identifiers

PMID32855719
PMCPMC7444344
OpenAlexW3047525197

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LicenceCC BY-NC-ND
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Registered trials

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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.