Evidence map›Paper›PMID 34628168›Full record

ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2021

Metformin to decrease COVID-19 severity and mortality: Molecular mechanisms and therapeutic potential.

Olexandr Kamyshnyi, Victoriya Matskevych, Tetyana Lenchuk, Olha Strilbytska, Kenneth Storey, Oleh Lushchak

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 3 syntheses or guidelines pooled it, 61 citations in OpenAlex.

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  18. The role of SARS-CoV-2-mediated NF-κB activation in COVID-19 patients.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
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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

6 authors at 4 institutions in 2 countries.

Olexandr KamyshnyiDepartment of Microbiology, Virology and Immunology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.
Victoriya MatskevychDepartment of Radiology and Radiation Medicine, Ivano-Frankivsk National Medical University, Ivano-Frankivsk, Ukraine.
Tetyana LenchukDepartment of Radiology and Radiation Medicine, Ivano-Frankivsk National Medical University, Ivano-Frankivsk, Ukraine.
Olha StrilbytskaDepartment of Biochemistry and Biotechnology, Vasyl Stefanyk Precarpathian National University, Ivano-Frankivsk, Ukraine.
Kenneth StoreyDepartment of Biology, Carleton University, Ottawa, Canada.
Oleh LushchakDepartment of Biochemistry and Biotechnology, Vasyl Stefanyk Precarpathian National University, Ivano-Frankivsk, Ukraine; Research and Development University, Ivano-Frankivsk, Ukraine. Electronic address: oleh.lushchak@pnu.edu.ua.
Ivano-Frankivsk National Medical University · UACarleton University · CAI.Horbachevsky Ternopil National Medical University · UAVasyl Stefanyk Precarpathian National University · UA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic caused by the coronavirus SARS-CoV-2 has become a serious challenge for medicine and science. Analysis of the molecular mechanisms associated with the clinical manifestations and severity of COVID-19 has identified several key points of immune dysregulation observed in SARS-CoV-2 infection. For diabetic patients, factors including higher binding affinity and virus penetration, decreased virus clearance and decreased T cell function, increased susceptibility to hyperinflammation, and cytokine storm may make these patients susceptible to a more severe course of COVID-19 disease. Metabolic changes induced by diabetes, especially hyperglycemia, can directly affect the immunometabolism of lymphocytes in part by affecting the activity of the mTOR protein kinase signaling pathway. High mTOR activity can enhance the progression of diabetes due to the activation of effector proinflammatory subpopulations of lymphocytes and, conversely, low activity promotes the differentiation of T-regulatory cells. Interestingly, metformin, an extensively used antidiabetic drug, inhibits mTOR by affecting the activity of AMPK. Therefore, activation of AMPK and/or inhibition of the mTOR-mediated signaling pathway may be an important new target for drug therapy in COVID-19 cases mostly by reducing the level of pro-inflammatory signaling and cytokine storm. These suggestions have been partially confirmed by several retrospective analyzes of patients with diabetes mellitus hospitalized for severe COVID-19.

Indexed as

COVID-19 Drug TreatmentSeverity of Illness IndexCOVID-19Diabetes MellitusHumansHypoglycemic AgentsImmunity, CellularLymphocytesMetforminMortalityT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesHypoglycemic AgentsMetforminMTOR protein, humanTOR Serine-Threonine KinasesCOVID-19ImmunometabolismLymphocytesMetformin

Identifiers

PMID34628168
PMCPMC8492612
OpenAlexW3204168235

What OpenQuestion holds

Texttitle and abstract
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.