Evidence map›Paper›PMID 34012406›Full record

ArticleFrontiers in physiology2021

Metformin

Xia Dong, Tiankun Hui, Jie Chen, Zheng Yu, Dongyan Ren, Suqi Zou, Shunqi Wang, Erkang Fei, Huifeng Jiao, Xinsheng Lai

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Xia DongSchool of Basic Medical Sciences, Nanchang University, Nanchang, China.
Tiankun HuiLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Jie ChenLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Zheng YuLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Dongyan RenLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Suqi ZouLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Shunqi WangLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Erkang FeiLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Huifeng JiaoSchool of Basic Medical Sciences, Nanchang University, Nanchang, China.
Xinsheng LaiLaboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang, China.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a genetic neuromuscular disease characterized by progressive muscle weakness and wasting. Stimulation of AMP-activated protein kinase (AMPK) has been demonstrated to increase muscle function and protect muscle against damage in dystrophic mice. Metformin is a widely used anti-hyperglycemic drug and has been shown to be an indirect activator of AMPK. Based on these findings, we sought to determine the effects of metformin on neuromuscular deficits in mdx murine model of DMD. In this study, we found metformin treatment increased muscle strength accompanied by elevated twitch and tetanic force of tibialis anterior (TA) muscle in mdx mice. Immunofluorescence and electron microscopy analysis of metformin-treated mdx muscles revealed an improvement in muscle fiber membrane integrity. Electrophysiological studies showed the amplitude of miniature endplate potentials (mEPP) was increased in treated mice, indicating metformin also improved neuromuscular transmission of the mdx mice. Analysis of mRNA and protein levels from muscles of treated mice showed an upregulation of AMPK phosphorylation and dystrophin-glycoprotein complex protein expression. In conclusion, metformin can indeed improve muscle function and diminish neuromuscular deficits in mdx mice, suggesting its potential use as a therapeutic drug in DMD patients.

Indexed as

AMP-activated protein kinaseDuchenne muscular dystrophymetforminneuromuscular junctionskeletal muscle

Identifiers

PMID34012406
PMCPMC8126699
OpenAlexW3158671034

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.