Evidence map›Paper›PMID 32492904›Full record

ArticleJournal of clinical medicine2020

The Anti-Diabetic Drug Metformin Rescues Aberrant Mitochondrial Activity and Restrains Oxidative Stress in a Female Mouse Model of Rett Syndrome.

Ilaria Zuliani, Chiara Urbinati, Daniela Valenti, Maria Cristina Quattrini, Vanessa Medici, Livia Cosentino, Donatella Pietraforte, Fabio Di Domenico, Marzia Perluigi, Rosa Anna Vacca and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-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

20 citing papers in PubMed, 32 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

11 authors at 3 institutions in 1 country.

Ilaria ZulianiDepartment of Biochemical Sciences, Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0001-9723-3780
Chiara UrbinatiCenter for Behavioral Sciences and Mental Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
Daniela ValentiInstitute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, 70126 Bari, Italy.
Maria Cristina QuattriniCore Facilities, Istituto Superiore di Sanità, 00161 Rome, Italy.
Vanessa MediciCenter for Behavioral Sciences and Mental Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
Livia CosentinoCenter for Behavioral Sciences and Mental Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
Donatella PietraforteCore Facilities, Istituto Superiore di Sanità, 00161 Rome, Italy.ORCID 0000-0001-6370-912X
Fabio Di DomenicoDepartment of Biochemical Sciences, Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0002-2013-209X
Marzia PerluigiDepartment of Biochemical Sciences, Sapienza University of Rome, 00185 Rome, Italy.
Rosa Anna VaccaInstitute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, 70126 Bari, Italy.ORCID 0000-0003-2438-6449
Bianca De FilippisCenter for Behavioral Sciences and Mental Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
Istituto Superiore di Sanità · ITSapienza University of Rome · ITInstitute of Biomembranes, Bioenergetics and Molecular Biotechnologies · IT

Funding

Italian Ministry of Health GR-2018-12366210
6 · The paper itself

Abstract

Metformin is the first-line therapy for diabetes, even in children, and a promising attractive candidate for drug repurposing. Mitochondria are emerging as crucial targets of metformin action both in the periphery and in the brain. The present study evaluated whether treatment with metformin may rescue brain mitochondrial alterations and contrast the increased oxidative stress in a validated mouse model of Rett syndrome (RTT), a rare neurologic disorder of monogenic origin characterized by severe behavioral and physiological symptoms. No cure for RTT is available. In fully symptomatic RTT mice (12 months old MeCP2-308 heterozygous female mice), systemic treatment with metformin (100 mg/kg ip for 10 days) normalized the reduced mitochondrial ATP production and ATP levels in the whole-brain, reduced brain oxidative damage, and rescued the increased production of reactive oxidizing species in blood. A 10-day long treatment with metformin also boosted pathways related to mitochondrial biogenesis and antioxidant defense in the brain of metformin-treated RTT mice. This treatment regimen did not improve general health status and motor dysfunction in RTT mice at an advanced stage of the disease. Present results provide evidence that systemic treatment with metformin may represent a novel, repurposable therapeutic strategy for RTT.

Indexed as

metforminNrf2PGC-1αrepurposingRett syndrome

Identifiers

PMID32492904
PMCPMC7355965
OpenAlexW3028691087

What OpenQuestion holds

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LicenceCC BY
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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.