Evidence map›Paper›PMID 29636010›Full record

ArticleBMC cardiovascular disorders2018

Metformin restores electrophysiology of small conductance calcium-activated potassium channels in the atrium of GK diabetic rats.

Xi Fu, Yilong Pan, Qian Cao, Bin Li, Shuo Wang, Hongjiao Du, Na Duan, Xiaodong Li

Open access · goldFull text read
In one paragraph

Article in BMC cardiovascular disorders, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 9% 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, 27 citations in OpenAlex.

  1. Role of epicardial adipose tissue in heart failure with preserved ejection fraction: An emerging molecular mechanism and therapeutic potential.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
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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

8 authors at 2 institutions in 1 country.

Xi FuDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Yilong PanDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Qian CaoDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Bin LiDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Shuo WangDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Hongjiao DuDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Na DuanDepartment of Cardiology, The People's Hospital of Liaoning Province, Shenyang, 110016, People's Republic of China.
Xiaodong LiDepartment of Cardiology, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China. lxd1894021@126.com.ORCID 0000-0002-8901-9896
China Medical University · CNLiaoning Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall conductance calcium-activated potassium channels (SK channels) play a critical role in action potential repolarization in cardiomyocytes. Recently, the potential anti-arrhythmic effect of metformin in diabetic patients has been recognized, yet the underlying mechanism remains elusive.

methodsDiabetic Goto-Kakizaki (GK) rats were untreated or treated with metformin (300 mg/kg/day) for 12 weeks, and age-matched Wistar rats were used as control (n = 6 per group). Electrocardiography, Hematoxylin-eosin staining and Masson's trichome staining were performed to assess cardiac function, histology and fibrosis. The expression levels of the SK channels in the myocardium were determined by real-time PCR and Western blotting. The electrophysiology of the SK channels in the cardiomyocytes isolated from the three groups of rats was examined by patch clamp assay, with specific blockade of the SK channels with apamin.

resultsMetformin treatment significantly reduced cardiac fibrosis and alleviated arrhythmia in the diabetic rats. In the atrial myocytes from control, GK and metformin-treated GK rats, the expression of KCa2.2 (SK2 channel) was down-regulated and the expression of KCa2.3 (SK3 channel) was up-regulated in the atrium of GK rats as compared with that of control rats, and metformin reversed diabetes-induced alterations in atrial SK channel expression. Moreover, patch clamp assay revealed that the SK current was markedly reduced and the action potential duration was prolonged in GK atrial myocytes, and the SK channel function was partially restored in the atrial myocytes from metformin-treated GK rats.

conclusionsOur data suggests an involvement of the SK channels in the development of arrhythmia under diabetic conditions, and supports a potential beneficial effect of metformin on atrial electrophysiology.

Indexed as

Action PotentialsAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacDiabetes MellitusDisease Models, AnimalHeart AtriaHeart RateHypoglycemic AgentsMaleMetforminMyocytes, CardiacRats, WistarSmall-Conductance Calcium-Activated Potassium ChannelsAnti-Arrhythmia AgentsHypoglycemic AgentsKcnn2 protein, ratKcnn3 protein, ratMetforminSmall-Conductance Calcium-Activated Potassium ChannelsArrhythmiaDiabetesMetforminSK channelSmall conductance calcium-activated potassium channel

Identifiers

PMID29636010
PMCPMC5894224
OpenAlexW2803912801

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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.