Evidence mapPaperPMID 32535544Full record

ReviewRedox biology2020

Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

Nadezda Apostolova, Francesca Iannantuoni, Aleksandra Gruevska, Jordi Muntane, Milagros Rocha, Victor M Victor

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 2 pooled it
8.7field-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

109 citing papers in PubMed, 2 syntheses or guidelines pooled it, 186 citations in OpenAlex.

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  20. RuvidarViruses · 2025
    Article

49 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

6 authors at 5 institutions in 1 country.

Nadezda ApostolovaDepartment of Pharmacology, University of Valencia - FISABIO (Foundation for the Promotion of Health and Biomedical Research in the Valencian Region), Valencia, Spain; CIBERehd (Biomedical Research Networking Centre on Hepatic and Digestive Diseases), Valencia, Spain. Electronic address: nadezda.apostolova@uv.es.
Francesca IannantuoniService of Endocrinology and Nutrition. University Hospital Doctor Peset, FISABIO, Valencia, Spain.
Aleksandra GruevskaDepartment of Pharmacology, University of Valencia - FISABIO (Foundation for the Promotion of Health and Biomedical Research in the Valencian Region), Valencia, Spain.
Jordi MuntaneInstitute of Biomedicine of Seville (IBiS), University Hospital "Virgen del Rocío"/CSIC/University of Seville, Seville, Spain.
Milagros RochaCIBERehd (Biomedical Research Networking Centre on Hepatic and Digestive Diseases), Valencia, Spain; Service of Endocrinology and Nutrition. University Hospital Doctor Peset, FISABIO, Valencia, Spain.
Victor M VictorCIBERehd (Biomedical Research Networking Centre on Hepatic and Digestive Diseases), Valencia, Spain; Service of Endocrinology and Nutrition. University Hospital Doctor Peset, FISABIO, Valencia, Spain; Department of Physiology, University of Valencia, Valencia, Spain. Electronic address: victor.victor@uv.es.
Universitat de València · ESCentre for Biomedical Network Research on Rare Diseases · ESFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ESHospital Universitario Doctor Peset · ESUniversidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin is still not fully understood. This review provides an overview of the existing literature concerning the beneficial mitochondrial and vascular effects of metformin, which it exerts by diminishing oxidative stress and reducing leukocyte-endothelium interactions. Specifically, we describe the molecular mechanisms involved in metformin's effect on gluconeogenesis, its capacity to interfere with major metabolic pathways (AMPK and mTORC1), its action on mitochondria and its antioxidant effects. We also discuss potential targets for therapeutic intervention based on these molecular actions.

Indexed as

Diabetes Mellitus, Type 2MetforminEndotheliumHumansLeukocytesMitochondriaMetforminAtherosclerosisMetforminMitochondriaOxidative stressPathophysiologyTreatmentType 2 diabetes

Identifiers

PMID32535544
PMCPMC7296337
OpenAlexW3028071487

What Socratic holds

Texttitle and abstract
LicenceCC BY-NC-ND
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 Socratic graph.