Evidence mapPaperPMID 32667970Full record

ArticleCardiovascular research2021

Metformin directly suppresses atherosclerosis in normoglycaemic mice via haematopoietic adenosine monophosphate-activated protein kinase.

Anusha Seneviratne, Luke Cave, Gareth Hyde, Soren Kragh Moestrup, David Carling, Justin C Mason, Dorian O Haskard, Joseph James Boyle

Open access · hybridFull text read
In one paragraph

Article in Cardiovascular research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  9. Metformin role in Parkinson's disease: a double-sword effect.Molecular and cellular biochemistry · 2024
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  13. Article
  14. Macrophage Phenotyping in Atherosclerosis by Proteomics.International journal of molecular sciences · 2023
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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.

Anusha SeneviratneNational Heart and Lung Institute, Imperial College London, London, UK.
Luke CaveNational Heart and Lung Institute, Imperial College London, London, UK.
Gareth HydeNational Heart and Lung Institute, Imperial College London, London, UK.
Soren Kragh MoestrupDepartment of Biomedicine, Aarhus University, Aarhus C, Denmark.
David CarlingMRC London Institute of Medical Sciences, Imperial College London, UK.
Justin C MasonNational Heart and Lung Institute, Imperial College London, London, UK.
Dorian O HaskardNational Heart and Lung Institute, Imperial College London, London, UK.
Joseph James BoyleNational Heart and Lung Institute, Imperial College London, London, UK.
Imperial College London · GBAarhus University · DKMRC London Institute of Medical Sciences · GB

Funding

Biotechnology and Biological Sciences Research Council BB/L015129/1British Heart Foundation FS/13/12/30037British Heart Foundation PG/15/57/31580British Heart Foundation PG/17/71/33242Medical Research Council MC_U120027537Medical Research Council MR/N011775/1Wellcome Trust 104931/Z/14/Z
6 · The paper itself

Abstract

aimsAtherosclerotic vascular disease has an inflammatory pathogenesis. Heme from intraplaque haemorrhage may drive a protective and pro-resolving macrophage M2-like phenotype, Mhem, via AMPK and activating transcription factor 1 (ATF1). The antidiabetic drug metformin may also activate AMPK-dependent signalling. Hypothesis: Metformin systematically induces atheroprotective genes in macrophages via AMPK and ATF1, thereby suppresses atherogenesis. METHODS AND

resultsNormoglycaemic Ldlr-/- hyperlipidaemic mice were treated with oral metformin, which profoundly suppressed atherosclerotic lesion development (P < 5 × 10-11). Bone marrow transplantation from AMPK-deficient mice demonstrated that metformin-related atheroprotection required haematopoietic AMPK [analysis of variance (ANOVA), P < 0.03]. Metformin at a clinically relevant concentration (10 μM) evoked AMPK-dependent and ATF1-dependent increases in Hmox1, Nr1h2 (Lxrb), Abca1, Apoe, Igf1, and Pdgf, increases in several M2-markers and decreases in Nos2, in murine bone marrow macrophages. Similar effects were seen in human blood-derived macrophages, in which metformin-induced protective genes and M2-like genes, suppressible by si-ATF1-mediated knockdown. Microarray analysis comparing metformin with heme in human macrophages indicated that the transcriptomic effects of metformin were related to those of heme, but not identical. Metformin-induced lesional macrophage expression of p-AMPK, p-ATF1, and downstream M2-like protective effects.

conclusionMetformin activates a conserved AMPK-ATF1-M2-like pathway in mouse and human macrophages, and results in highly suppressed atherogenesis in hyperlipidaemic mice via haematopoietic AMPK.

Indexed as

Plaque, AtheroscleroticActivating Transcription Factor 1AMP-Activated Protein KinasesAnimalsAortaAortic DiseasesAtherosclerosisCells, CulturedDisease Models, AnimalGene Expression RegulationHumansMacrophagesMetforminMiceMice, KnockoutPhenotypeActivating Transcription Factor 1AMP-Activated Protein KinasesATF1 protein, humanAtf1 protein, mouseMetforminReceptors, LDLAMPKAtherosclerosisGene expressionMacrophageMetforminTranscription factor

Identifiers

PMID32667970
PMCPMC8064441
OpenAlexW3043760418

What Socratic holds

Textfull text, public
LicenceCC BY
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Registered trials

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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.