Evidence map›Paper›PMID 39412170›Full record

ReviewLiver international : official journal of the International Association for the Study of the Liver2025

Impact of PNPLA3 I148M on Clinical Outcomes in Patients With MASLD.

Salvatore Petta, Angelo Armandi, Elisabetta Bugianesi

Erratum issuedAbstract readReview
In one paragraph

Review in Liver international : official journal of the International Association for the Study of the Liver, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Correction to 'Impact of PNPLA3 I148M on Clinical Outcomes in Patients With MASLD'.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  2. Observational
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Linked Intronic Polymorphisms of theInternational journal of molecular sciences · 2026
    Article
  9. Review
  10. Review
  11. Clinical and Genetic Predictors of Non-Alcoholic Steatotic Liver Disease and Fibrosis in Lean Individuals.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  12. Article
  13. Article
  14. MetALD: New Perspectives on an Old Overlooked Disease.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  15. Review
  16. Article
  17. The Role of Exercise in Steatotic Liver Diseases: An Updated Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  18. Article
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Salvatore PettaSezione di Gastroenterologia, Di.Bi.M.I.S, University of Palermo, Palermo, Italy.ORCID 0000-0002-0822-9673
Angelo ArmandiDivision of Gastroenterology and Hepatology, Department of Medical Sciences, University of Turin, Turin, Italy.ORCID 0000-0002-7245-4445
Elisabetta BugianesiDivision of Gastroenterology and Hepatology, Department of Medical Sciences, University of Turin, Turin, Italy.

Funding

PNRR "D3 4 Health - Digital Driven Diagnostics, prognostics and therapeutics for sustainable Health care"PNRR M4C2I1.3PNRR-MAD-2022-12375656PRIN 2022 2022L273C9RF-2021-12372399
6 · The paper itself

Abstract

BACKGROUND AND

aimsMetabolic dysfunction-associated steatotic liver disease (MASLD) is a heterogenous clinical and histopathological entity, where multiple metabolic co-factors are intertwined with high interindividual variability. The impact and severity of each factor (including obesity and type 2 diabetes) define a systemic dysmetabolism that can lead to either advanced liver disease and its complication (including hepatocellular carcinoma and clinical events related to portal hypertension) or extrahepatic events: incident cardiovascular disease, chronic kidney disease and extrahepatic cancers. The balance between environmental factors and genetic susceptibility has unique implications in MASLD: the intermittent injury of metabolic co-factors, their fluctuation over time and their specific management, are counterbalanced by the presence of gene variants that can significantly impact the disease at multiple levels. The I148M variant in the PNPLA3 gene is the most investigated genetic susceptibility that induces a more severe steatohepatitis, enhanced fibrogenesis and can shape the incidence of long-term clinical events regardless of, or worsened by, other metabolic risk factors. METHODS AND

resultsIn this review, we will summarise the updated evidence on the natural history of MASLD accounting for classical metabolic risk factors, the role of PNPLA3 in clinical sub-phenotyping (e.g., 'lean MASLD'), impact on disease severity and fibrosis progression, as well as its role for prognostication, alone or in combination with non-invasive tools into polygenic risk scores.

Indexed as

Fatty LiverLipaseMembrane ProteinsNon-alcoholic Fatty Liver DiseaseAcyltransferasesDisease ProgressionGenetic Predisposition to DiseaseHumansPhospholipases A2, Calcium-IndependentRisk FactorsAcyltransferasesLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humancardiovascular diseasehepatocellular carcinomaliver fibrosismetabolic dysfunction‐associated Steatotic liver diseasemetabolic syndromePNPLA3portal hypertensionsingle nucleotide polymorphisms

Identifiers

PMID39412170
PMCPMC11815615

What OpenQuestion holds

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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.