Evidence map›Paper›PMID 39092773›Full record

ReviewImmunity, inflammation and disease2024

Pharmacological characterization of the antidiabetic drug metformin in atherosclerosis inhibition: A comprehensive insight.

Areej Turkistani, Haydar M Al-Kuraishy, Ali I Al-Gareeb, Athanasios Alexiou, Marios Papadakis, Mostafa M Bahaa, Salah Al-Windy, Gaber El-Saber Batiha

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Trial
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  3. Evaluation of metformin's effect on 5-fluorouracil-induced cardiotoxicity through cellular protection.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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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

8 authors.

Areej TurkistaniDepartment of Pharmacology and Toxicology, College of Medicine, Taif University, Taif, Saudi Arabia.
Haydar M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ali I Al-GareebDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Athanasios AlexiouDepartment of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, New South Wales, Australia.
Marios PapadakisDepartment of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Wuppertal, Germany.
Mostafa M BahaaPharmacy Practice Department, Faculty of Pharmacy, Horus University, New Damietta, Egypt.ORCID 0000-0003-3332-4573
Salah Al-WindyDepartment of Biology, College of Science, Baghdad University, Baghdad, Iraq.
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, Egypt.

Funding

Universität Witten/Herdecke
6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is a progressive disease that interferes with blood flow, leading to cardiovascular complications such as hypertension, ischemic heart disease, ischemic stroke, and vascular ischemia. The progression of AS is correlated with inflammation, oxidative stress, and endothelial dysfunction. Various signaling pathways, like nuclear erythroid-related factor 2 (Nrf2) and Kruppel-like factor 2 (KLF2), are involved in the pathogenesis of AS. Nrf2 and KLF2 have anti-inflammatory and antioxidant properties. Thus, activation of these pathways may reduce the development of AS. Metformin, an insulin-sensitizing drug used in the management of type 2 diabetes mellitus (T2DM), increases the expression of Nrf2 and KLF2. AS is a common long-term macrovascular complication of T2DM. Thus, metformin, through its pleiotropic anti-inflammatory effect, may attenuate the development and progression of AS.

aimsTherefore, this review aims to investigate the possible role of metformin in AS concerning its effect on Nrf2 and KLF2 and inhibition of reactive oxygen species (ROS) formation. In addition to its antidiabetic effect, metformin can reduce cardiovascular morbidities and mortalities compared to other antidiabetic agents, even with similar blood glucose control by the Nrf2/KLF2 pathway activation.

conclusionIn conclusion, metformin is an effective therapeutic strategy against the development and progression of AS, mainly through activation of the KLF2/Nrf2 axis.

Indexed as

AtherosclerosisDiabetes Mellitus, Type 2Hypoglycemic AgentsKruppel-Like Transcription FactorsMetforminNF-E2-Related Factor 2AnimalsHumansOxidative StressReactive Oxygen SpeciesSignal TransductionHypoglycemic AgentsKLF2 protein, humanKruppel-Like Transcription FactorsMetforminNFE2L2 protein, humanNF-E2-Related Factor 2Reactive Oxygen SpeciesatherosclerosisKruppel like factor 2metforminnuclear erythroid related factor 2

Identifiers

PMID39092773
PMCPMC11295104

What Socratic holds

Texttitle and abstract
LicenceCC BY
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.