Evidence map›Paper›PMID 42366560›Full record

ReviewClinical and molecular hepatology2026

Genetic and genomic insights across the steatotic liver disease spectrum.

Jake P Mann, Karn Wijarnpreecha, Vitchapong Prasitsumrit, Eric Trépo, Elizabeth K Speliotes, Vincent L Chen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and molecular hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Jake P MannDepartment of Immunology & Immunotherapy, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, Birmingham, UK.
Karn WijarnpreechaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Banner University Medical Center, Phoenix, AZ, USA.
Vitchapong PrasitsumritDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Eric TrépoDepartment of Gastroenterology, Hepatopancreatology and Digestive Oncology, Hôpital Universitaire de Bruxelles, Université Libre de Bruxelles, Brussels, Belgium.
Elizabeth K SpeliotesDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Vincent L ChenDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA. vichen@umich.edu.

Funding

Integrative Polygenic Genetic Studies of Non-alcoholic Fatty Liver DiseaseR01DK131787 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SPELIOTES, ELIZABETH K · 2022 to 2025
$2.7M
Identification and Characterization of Loci Associated with Non-alcoholic Fatty Liver DiseaseR01DK128871 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ALLRED, NICHOLETTE D., SPELIOTES, ELIZABETH K · 2021 to 2024
$2.6M
Multi Ancestry Whole Genome Sequencing Analyses of MASLD with Functional Follow UpR01DK141823 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Nicholette D. Allred, Elizabeth K Speliotes · 2025 to 2026
$1.5M
Predictive models for incident cirrhosis in non-alcoholic fatty liver disease using genetic and electronic medical record-based risk factorsK08DK132312 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Vincent Lingzhi Chen · 2022 to 2026
$834k
Action Medical Research GN4039AstraZenecaBirmingham Health PartnersGlaxoSmithKlineIpsenKOWANIH HHS K08 DK132312NIH HHS R01 DK128871NIH HHS R01 DK131787NIH HHS R01 DK141823University of Michigan Department of Internal Medicine
6 · The paper itself

Abstract

Chronic liver disease is a rapidly growing cause of morbidity and mortality worldwide, and this increase is largely driven by steatotic liver disease (SLD) comprising metabolic dysfunction-associated steatotic liver disease (MASLD), alcohol-related liver disease (ALD), and MASLD and increased alcohol intake (MetALD). Hepatic steatosis and fibrosis are highly heritable and genetic variation has also been associated with the risk of hepatocellular carcinoma (HCC) and hepatic decompensation. This review summarizes the state of the art of genetics and genomics in SLD, with particular emphasis on potential clinical utility. Variants in/near genes including PNPLA3, TM6SF2, and HSD17B13 have been associated with cirrhosis and HCC in both MASLD and ALD, while others such as those in GCKR, TRIB1, and GPAM have been consistently associated with greater risk of hepatic steatosis in MASLD with much weaker effects if any on cirrhosis and HCC. While data on MetALD genetics are limited, we believe that the genetic risk factors for liver steatosis, cirrhosis, and HCC will be similar in MetALD compared to MASLD and ALD based on the largely shared genetic risk factors for MASLD and ALD. Finally, we discuss future directions in SLD genetics, notably genetically-defined disease subtypes, gene-environment interactions and their implications for therapy, and the utility of genetics in clinical risk stratification. Genetic studies have provided insight into important disease processes in SLD and may have an upcoming role in clinical care.

Indexed as

Fatty Liver17-Hydroxysteroid DehydrogenasesAcyltransferasesCarcinoma, HepatocellularGenetic Predisposition to DiseaseGenomicsHumansLipaseLiver CirrhosisLiver NeoplasmsMembrane ProteinsPhospholipases A2, Calcium-IndependentRisk Factors17-Hydroxysteroid DehydrogenasesAcyltransferasesLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanGene therapyPrognosisSNPTreatment response

Identifiers

PMID42366560

What Socratic 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 Socratic graph.