Evidence map›Paper›PMID 24222941›Full record

ReviewWorld journal of gastroenterology2013

PNPLA3 I148M polymorphism and progressive liver disease.

Paola Dongiovanni, Benedetta Donati, Roberta Fares, Rosa Lombardi, Rosellina Margherita Mancina, Stefano Romeo, Luca Valenti

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 3 pooled it
13.6field-weighted citation impact, top 1% 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

132 citing papers in PubMed, 3 syntheses or guidelines pooled it, 246 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  7. The Human PNPLA3FASEB bioAdvances · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Fifteen Years of PNPLA3: Transforming Hepatology Through Human Genetics.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  19. Contribution ofInternational journal of molecular sciences · 2025
    Article
  20. Gene-based therapies for steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review

72 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Paola DongiovanniPaola Dongiovanni, Benedetta Donati, Roberta Fares, Rosa Lombardi, Luca Valenti, Internal Medicine, Fondazione IRCCS Ca' Granda Ospedale Policlinico Milano, Department of Pathophysiology and Transplantation, Università degli Studi di Milano, 20122 Milano, Italy.
Benedetta Donati
Roberta Fares
Rosa Lombardi
Rosellina Margherita Mancina
Stefano Romeo
Luca Valenti
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 148 Isoleucine to Methionine protein variant (I148M) of patatin-like phospholipase domain-containing 3 (PNPLA3), a protein is expressed in the liver and is involved in lipid metabolism, has recently been identified as a major determinant of liver fat content. Several studies confirmed that the I148M variant predisposes towards the full spectrum of liver damage associated with fatty liver: from simple steatosis to steatohepatitis and progressive fibrosis. Furthermore, the I148M variant represents a major determinant of progression of alcohol related steatohepatitis to cirrhosis, and to influence fibrogenesis and related clinical outcomes in chronic hepatitis C virus hepatitis, and possibly chronic hepatitis B virus hepatitis, hereditary hemochromatosis and primary sclerosing cholangitis. All in all, studies suggest that the I148M polymorphism may represent a general modifier of fibrogenesis in liver diseases. Remarkably, the effect of the I148M variant on fibrosis was independent of that on hepatic steatosis and inflammation, suggesting that it may affect both the quantity and quality of hepatic lipids and the biology of non-parenchymal liver cells besides hepatocytes, directly promoting fibrogenesis. Therefore, PNPLA3 is a key player in liver disease progression. Assessment of the I148M polymorphism will possibly inform clinical practice in the future, whereas the determination of the effect of the 148M variant will reveal mechanisms involved in hepatic fibrogenesis.

Indexed as

Polymorphism, GeneticAcyltransferasesCarcinoma, HepatocellularCholangitis, SclerosingDisease ProgressionFatty LiverFatty Liver, AlcoholicGenetic Predisposition to DiseaseHemochromatosisHepatitis B, ChronicHepatitis C, ChronicHumansLipaseLiver CirrhosisLiver Cirrhosis, AlcoholicLiver NeoplasmsAcyltransferasesLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanAlcoholic liver diseaseChronic hepatitis C virus hepatitisFibrogenesisGeneticsHepatocellular carcinomaLiver diseaseNonalcoholic fatty liver diseasePatatin-like phospholipase domain-containing 3Single nucleotide polymorphismSteatosis

Identifiers

PMID24222941
PMCPMC3819533
OpenAlexW2031119940

What OpenQuestion holds

Textmetadata
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.