ArticleJHEP reports : innovation in hepatology2026
Article in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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.
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Who cites it
6 citing papers in PubMed.
- Cardiovascular-Kidney-Metabolic Syndrome and Its Hepatic Dimension: A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Genetic and genomic insights across the steatotic liver disease spectrum.Clinical and molecular hepatology · 2026Review
- Genetic Impacts on Variability of Body Fat Distribution Uncover Gene-Environment and Gene-Gene Interactions.bioRxiv : the preprint server for biology · 2026Article
- Reply to: "Gene-environment "amplification" of liver stiffness requires more clinically meaningful analytic approaches".JHEP reports : innovation in hepatology · 2026Article
- Gene-environment "amplification" of liver stiffness requires more clinically meaningful analytic approaches.JHEP reports : innovation in hepatology · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background & Aims: Genetic predisposition (especially variants in Methods: We cross-sectionally analyzed data from two cohorts: patients referred to tertiary liver care (N = 1,554) and individuals at risk for SLD (N = 1,728). Multivariable regression models with and without interaction terms were used to assess the independent and interactive effects of genetic risk variants, metabolic dysfunction (HOMA-IR, BMI), and alcohol intake on liver fibrosis severity as assessed by liver stiffness measurement (LSM). Results: Mean age was 52 and 56 years in the Tertiary-care cohort and the At-risk cohort, respectively. Most participants were male, 23% and 53% suffered from obesity, and 39% and 58% were categorized as insulin resistant, respectively. Median LSM was 5.5 kPa and 4.7 kPa, with 21% and 9.6% having LSM ≥8 kPa, respectively. In total, 48% and 44% carried at least one Conclusions: Our findings indicate that Impact and implications: Our findings indicate that fibrosis progression in steatotic liver disease is mediated by an interaction of environmental risk factors (obesity, insulin resistance, alcohol consumption) and genetic risk variants, such as
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Registered trials
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.