Evidence map›Paper›PMID 39560367›Full record

ArticleJournal of internal medicine2025

Statin-associated regulation of hepatic PNPLA3 in patients without known liver disease.

Osman Ahmed, Vladimir S Shavva, Laura Tarnawski, Wanmin Dai, Filip Borg, Viggo V Olofsson, Ting Liu, Peter Saliba-Gustafsson, Christian Simini, Matteo Pedrelli and 8 more

Abstract read
In one paragraph

Article in Journal of internal medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

18 authors.

Osman AhmedDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0002-2854-2552
Vladimir S ShavvaDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Laura TarnawskiDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Wanmin DaiDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Filip BorgDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Viggo V OlofssonDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Ting LiuDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Peter Saliba-GustafssonCardio Metabolic Unit, Department of Laboratory Medicine, and Department of Medicine at Huddinge, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0002-7807-9009
Christian SiminiCardio Metabolic Unit, Department of Laboratory Medicine, and Department of Medicine at Huddinge, Karolinska Institutet, Stockholm, Sweden.
Matteo PedrelliCardio Metabolic Unit, Department of Laboratory Medicine, and Department of Medicine at Huddinge, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0003-0771-0569
Otto BergmanDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Giuseppe Danilo NorataDepartment of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, Milan, Italy.
Paolo PariniCardio Metabolic Unit, Department of Laboratory Medicine, and Department of Medicine at Huddinge, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0002-6541-8542
Anders Franco-CerecedaDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Per ErikssonDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0002-5635-2692
Stephen G MalinDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Hanna M BjörckDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Peder S OlofssonDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.

Funding

EUROPEAID 173691/DD/ACT/XK NanokosMedTechLabs and NovoNordiskNovo Nordisk fellowship and Stiftelsen Professor Nanna Svartz fondPNRR Missione 4PNRR Missione 6 PNRR-MAD-2022-12375913Progetti di Rilevante Interesse Nazionale PRIN 2017 K55HLCRicerca Finalizzata, Ministry of Health RF-2019-12370896Swedish Heart-Lung Foundation 20180451,20230006,20180072,21210524,20200827Swedish Research Council 2020-01442,2021-00500,2020-02583
6 · The paper itself

Abstract

BACKGROUND AND

objectivesStatins are used for metabolic dysfunction-associated steatotic liver disease (MASLD) (NAFLD) treatment, but their role in this context is unclear. Genetic variants of patatin-like phospholipase domain containing 3 (PNPLA3) are associated with MASLD susceptibility and statin treatment efficacy. Access to liver biopsies before established MASLD is limited, and statins and PNPLA3 in early liver steatosis are thus difficult to study.

methodsLiver biopsies were collected from 261 patients without known liver disease at surgery and stratified based on statin use and criteria for the metabolic syndrome (MS). Genotypes and transcript levels were measured using Illumina and Affymetrix arrays, and metabolic and lipoprotein profiles by clinical assays. Statin effects on PNPLA3, de novo lipogenesis (DNL), and lipid accumulation were further studied in vitro.

resultsThe PNPLA3

conclusionsCollectively, these observations suggest statin-associated regulation of PNPLA3 and DNL in liver. The potential interaction between PNPLA3 genotype and metabolic status should be considered in future studies in the context of statin therapy for MASLD.

Indexed as

Hydroxymethylglutaryl-CoA Reductase InhibitorsLipaseLipogenesisLiverMembrane ProteinsAcyltransferasesAdultFemaleGenotypeHumansMaleMetabolic SyndromeMiddle AgedNon-alcoholic Fatty Liver DiseasePhospholipases A2, Calcium-IndependentAcyltransferasesHydroxymethylglutaryl-CoA Reductase InhibitorsLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanlipogenesisMASLDmetabolic syndromeNAFLD

Identifiers

PMID39560367
PMCPMC11636427

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Texttitle and abstract
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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 OpenQuestion graph.