ArticleHepatology (Baltimore, Md.)2014
Hepatic gene expression profiles differentiate presymptomatic patients with mild versus severe nonalcoholic fatty liver disease.
Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers, 5 of them syntheses that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
204 citing papers in PubMed, 5 syntheses or guidelines pooled it, 317 citations in OpenAlex.
- Conserved hepatic RNA signatures across multiple cohorts reveal novel mechanistic clues for advanced fibrosis in human MASLD.Hepatology communications · 2026Pooled it
- Comprehensive meta-analysis reveals distinct gene expression signatures of MASLD progression.Life science alliance · 2024Pooled it
- Clinically important alterations in pharmacogene expression in histologically severe nonalcoholic fatty liver disease.Nature communications · 2023Pooled it
- Key hepatic signatures of human and mouse nonalcoholic steatohepatitis: A transcriptome-proteome data meta-analysis.Frontiers in endocrinology · 2022Pooled it
- Human hepatic gene expression signature of non-alcoholic fatty liver disease progression, a meta-analysis.Scientific reports · 2017Pooled it
- Treatment response in the PIVENS trial is associated with decreased Hedgehog pathway activity.Hepatology (Baltimore, Md.) · 2015Trial
- Sulfur amino acid restriction prevents S-adenosylmethionine-driven liver steatosis, hepatocellular carcinoma, and metabolic remodeling in high-fat-fed GNMT-null mice.bioRxiv : the preprint server for biology · 2026Article
- Integrative multi-omics analysis identifies stellate cell-derived complement component 7 as a predictor of fibrosis and liver-related events in MASLD.JHEP reports : innovation in hepatology · 2026Article
- A data-driven framework reconstructs the molecular continuum of human MASLD progression.Nature metabolism · 2026Article
- Development and clinical validation of a novel protein biomarkers-based algorithm for risk prediction and diagnosis of advanced liver fibrosis: a multi-centre study.Journal of advanced research · 2026Article
- Multi-omics investigation into the role of PTK7 as a driver of liver fibrosis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Potential Therapeutic Strategies for Steatosis, Oxidative Stress, Inflammation, and Fibrosis in Liver Disease.International journal of molecular sciences · 2026Review
- MASH-GA: a manually curated cross-species transcriptomic database for metabolic-associated steatohepatitis.Database : the journal of biological databases and curation · 2026Article
- Plasma Fibulin-5 as a Novel Marker for Advanced Fibrosis in Chronic Hepatitis C.Gastro hep advances · 2026Article
- CCL20-CCR6 axis mediates mucosal-associated invariant T-M2 macrophage crosstalk to drive immune dysregulation in liver cirrhosis.Frontiers in immunology · 2026Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- Plasticity of Epigenomic and Transcriptomic Aging Reveals Common Targets for Reprogramming by Environmental Exposures.Research square · 2025Article
- Article
- Plasma Lipid Metabolites Differentiate Metabolic From Viral Chronic Liver Disease.The Journal of infectious diseases · 2025Article
- ECM1 expression in chronic liver disease: Regulation by EGF/STAT1 and IFNγ/NRF2 signalling.JHEP reports : innovation in hepatology · 2025Article
144 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledClinicians rely upon the severity of liver fibrosis to segregate patients with well-compensated nonalcoholic fatty liver disease (NAFLD) into subpopulations at high- versus low-risk for eventual liver-related morbidity and mortality. We compared hepatic gene expression profiles in high- and low-risk NAFLD patients to identify processes that distinguish the two groups and hence might be novel biomarkers or treatment targets. Microarray analysis was used to characterize gene expression in percutaneous liver biopsies from low-risk, "mild" NAFLD patients (fibrosis stage 0-1; n = 40) and high-risk, "severe" NAFLD patients (fibrosis stage 3-4; n = 32). Findings were validated in a second, independent cohort and confirmed by real-time polymerase chain reaction and immunohistochemistry (IHC). As a group, patients at risk for bad NAFLD outcomes had significantly worse liver injury and more advanced fibrosis (severe NAFLD) than clinically indistinguishable NAFLD patients with a good prognosis (mild NAFLD). A 64-gene profile reproducibly differentiated severe NAFLD from mild NAFLD, and a 20-gene subset within this profile correlated with NAFLD severity, independent of other factors known to influence NAFLD progression. Multiple genes involved with tissue repair/regeneration and certain metabolism-related genes were induced in severe NAFLD. Ingenuity Pathway Analysis and IHC confirmed deregulation of metabolic and regenerative pathways in severe NAFLD and revealed overlap among the gene expression patterns of severe NAFLD, cardiovascular disease, and cancer.
conclusionBy demonstrating specific metabolic and repair pathways that are differentially activated in livers with severe NAFLD, gene profiling identified novel targets that can be exploited to improve diagnosis and treatment of patients who are at greatest risk for NAFLD-related morbidity and mortality.
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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 Socratic graph.