Evidence map›Paper›PMID 31016544›Full record

ArticleJournal of molecular histology2019

Oligoprotective effect of metformin through the AMPK-dependent on restoration of mitochondrial hemostasis in the cuprizone-induced multiple sclerosis model.

Seyed Hossein Hosseini Largani, Maryam Borhani-Haghighi, Parichehr Pasbakhsh, Vahid Pirhajati Mahabadi, Saied Nekoonam, Elham Shiri, Iraj Ragerdi Kashani, Adib Zendehdel

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  7. Berberine-loaded iron oxide nanoparticles alleviate cuprizone-induced astrocytic reactivity in a rat model of multiple sclerosis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Seyed Hossein Hosseini LarganiDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Maryam Borhani-HaghighiDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Parichehr PasbakhshDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Vahid Pirhajati MahabadiNeuroscience Research Center, Iran University of Medical Sciences, Poursina Street, 1417613151, Tehran, Iran.
Saied NekoonamDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Elham ShiriDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Iraj Ragerdi KashaniDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. ragerdi@tums.ac.ir.
Adib ZendehdelInstitute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Tehran University of Medical Sciences · IRIran University of Medical Sciences · IRRWTH Aachen University · DE

Funding

Tehran University of Medical Sciences and Health Services Grant 95-03-30- 32879
6 · The paper itself

Abstract

Oxidative stress with mitochondrial defects has a central role in the development and deterioration of Multiple sclerosis (MS). According to new findings of the effects of metformin on mitochondrial function, has attracted a lot of attention. Furthermore, it is suggested that metformin exerts its beneficial influence through AMP-activated protein kinase (AMPK) pathway. In the current study, we investigated the possible protective effects of metformin on oxidative stress and mitochondrial function by activating the AMPK pathway in the cuprizone-induced demyelination. Mice were fed with cuprizone for 6 weeks. Animals simultaneously received metformin. After sacrificing animals, myelinations, and gliosis, changes in transcription factor and biochemical analysis were assessed. Transmission electron microscopy and luxol fast blue staining revealed that the myelinated axons within corpus callosum of cuprizone-induced demyelination animals increased after administration of metformin. Metformin also upregulated the expression of mitochondrial biogenesis genes. Furthermore, the biochemical analysis demonstrated that metformin ameliorated the oxidative stress induced by cuprizone. Immunohistochemistry analysis showed that astrogliosis and microgliosis were decreased after metformin administration while it enhanced the number of oligodendrocytes. Our data implicated that metformin exerts its therapeutic effects on MS by AMPK signaling improved mitochondrial homeostasis and protected oligodendrocytes.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsAxonsCuprizoneDemyelinating DiseasesDisease Models, AnimalHemostasisHumansMetforminMiceMitochondriaMultiple SclerosisOligodendrogliaOxidative StressProtein KinasesSignal TransductionAMP-Activated Protein Kinase KinasesCuprizoneMetforminProtein KinasesAMP-activated protein kinase (AMPK)CuprizoneMetforminMitochondriaMultiple sclerosisOxidative stress

Identifiers

PMID31016544
OpenAlexW2942261628

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.