Evidence map›Paper›PMID 27167128›Full record

ArticleMolecular neurobiology2017

Metformin Improves Functional Recovery After Spinal Cord Injury via Autophagy Flux Stimulation.

Di Zhang, Jun Xuan, Bin-Bin Zheng, Yu-Long Zhou, Yan Lin, Yao-Sen Wu, Yi-Fei Zhou, Yi-Xing Huang, Quan Wang, Li-Yan Shen and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 3 pooled it
11.0field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 3 syntheses or guidelines pooled it, 137 citations in OpenAlex.

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23 more citing papers are in PubMed but not listed here.

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

16 authors at 2 institutions in 1 country.

Di ZhangDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Jun XuanDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Bin-Bin ZhengDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Yu-Long ZhouDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Yan LinDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Yao-Sen WuDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Yi-Fei ZhouDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Yi-Xing HuangDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Quan WangDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Li-Yan ShenDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Cong MaoDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Yan WuDepartment of Orthopaedics, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310058, Zhejiang Province, China.
Xiang-Yang WangDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China.
Nai-Feng TianDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China. fengnq@163.com.
Hua-Zi XuDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China. spinexu@163.com.
Xiao-Lei ZhangDepartment of Orthopaedics, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang Province, China. callmeroger@126.com.
Wenzhou Medical University · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal cord injury (SCI) is a severe neurological disease with few efficacious drugs. Autophagy is a cellular process to confront with stress after SCI and considered to be a therapeutic target of SCI. In this study, we investigated the therapeutic effect of metformin on functional recovery after SCI and its underlying mechanism of autophagy regulation. Using a rat model of traumatic SCI, we found improved function recovery which was paralleled by a reduction of apoptosis after metformin treatment. We further examined autophagy via detecting autophagosomes by transmission electron microscopy and immunofluorescence, as well as autophagy markers by western blot in each groups. The results showed that the number of autophagosomes and expression of autophagy markers such as LC3 and beclin1 were increased in SCI group, while autophagy substrate protein p62 as well as ubiquitinated proteins were found to accumulate in SCI group, indicating an impaired autophagy flux in SCI. But, metformin treatment attenuated the accumulation of p62 and ubiquitinated proteins, suggesting a stimulative effect of autophagy flux by metformin. Blockage of autophagy flux by chloroquine partially abolished the apoptosis inhibition and functional recovery effect of metformin on SCI, which suggested that the protective effect of metformin on SCI was through autophagy flux stimulation. Activation of AMPK as well as inhibition of its downstream mTOR signaling were detected under metformin treatment in vivo and in vitro; inhibition of AMPK signaling by compound C suppressed autophagy flux induced by metformin in vitro, indicating that AMPK signaling was involved in the effect of metformin on autophagy flux regulation. Together, these results illustrated that metformin improved functional recovery effect through autophagy flux stimulation and implied metformin to be a potential drug for SCI therapy.

Indexed as

AutophagyRecovery of FunctionAdenylate KinaseAnimalsApoptosisAutophagosomesEnzyme ActivationFemaleLysosomesMetforminModels, BiologicalNeuronsPC12 CellsRatsRats, Sprague-DawleySpinal Cord InjuriesAdenylate KinaseMetforminTOR Serine-Threonine KinasesAMPKApoptosisAutophagy fluxMetforminSpinal cord injury

Identifiers

PMID27167128
OpenAlexW2393553112

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.