ArticleHepatology communications2022
Distinct Hepatic Gene-Expression Patterns of NAFLD in Patients With Obesity.
Article in Hepatology communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- A distinct form of fat fibrosis is linked to insulin resistance in people with HIV.JCI insight · 2026Observational
- Effects of TNF-α in Human Precision-Cut Liver Slices and its Implications for Metabolic Dysfunction-Associated Steatohepatitis Progression.Inflammation · 2026Article
- Metabolic disease variants rewire gene regulation through disruption of DNA G-quadruplex structures.Genome biology · 2026Article
- Multiplexed targeted mRNA profiling of alcohol-related liver disease reveals stage-specific dysregulation of signaling pathways.Molecular biology reports · 2026Article
- Chemokines and chemokine receptors in metabolic dysfunction-associated steatohepatitis: pathogenic mechanisms and clinical implications.Cellular & molecular biology letters · 2026Review
- Article
- Diacerein improves liver fibrosis, steatosis, and atherosclerosis in ApoE knockout mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Spatial phosphoproteomics reveals regional phosphorylation features in liver cirrhosis progression.Journal of translational medicine · 2026Article
- Differences in gene expression may contribute to the racial differences in the risk of MASLD.PloS one · 2026Article
- Integrated analysis of RNA-binding proteins in MAFLD: mechanistic insights and diagnostic biomarker potential via alternative splicing.Journal of bioenergetics and biomembranes · 2025Article
- Will a "multivitamin" a day keep the "MASLD doctor" away?Metabolism and target organ damage · 2025Article
- Obesity-related drug-metabolizing enzyme expression alterations in the human liver.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Ablation of Hepatic Asah1 Gene Disrupts Hepatic Lipid Homeostasis and Promotes Fibrotic Nonalcoholic Steatohepatitis in Mice.The American journal of pathology · 2025Article
- Estrogen-dependent activation of TRX2 reverses oxidative stress and metabolic dysfunction associated with steatotic disease.Cell death & disease · 2025Article
- Hub Genes Involved in the Progression of Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma.Current medicinal chemistry · 2025Article
- Hepatocyte nuclear factor 4α is a critical factor for the production of complement components in the liver.In vitro cellular & developmental biology. Animal · 2024Article
- A male mouse model for metabolic dysfunction-associated steatotic liver disease and hepatocellular carcinoma.Nature communications · 2024Article
- Detection of early-stage NASH using non-invasive hyperpolarizedScientific reports · 2024Article
- Noninvasive assessment of organ-specific and shared pathways in multi-organ fibrosis using T1 mapping.Nature medicine · 2024Article
- Multiomics Picture of Obesity in Young Adults.Biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
Approaches to manage nonalcoholic fatty liver disease (NAFLD) are limited by an incomplete understanding of disease pathogenesis. The aim of this study was to identify hepatic gene-expression patterns associated with different patterns of liver injury in a high-risk cohort of adults with obesity. Using the NanoString Technologies (Seattle, WA) nCounter assay, we quantified expression of 795 genes, hypothesized to be involved in hepatic fibrosis, inflammation, and steatosis, in liver tissue from 318 adults with obesity. Liver specimens were categorized into four distinct NAFLD phenotypes: normal liver histology (NLH), steatosis only (steatosis), nonalcoholic steatohepatitis without fibrosis (NASH F0), and NASH with fibrosis stage 1-4 (NASH F1-F4). One hundred twenty-five genes were significantly increasing or decreasing as NAFLD pathology progressed. Compared with NLH, NASH F0 was characterized by increased inflammatory gene expression, such as gamma-interferon-inducible lysosomal thiol reductase (IFI30) and chemokine (C-X-C motif) ligand 9 (CXCL9), while complement and coagulation related genes, such as C9 and complement component 4 binding protein beta (C4BPB), were reduced. In the presence of NASH F1-F4, extracellular matrix degrading proteinases and profibrotic/scar deposition genes, such as collagens and transforming growth factor beta 1 (TGFB1), were simultaneously increased, suggesting a dynamic state of tissue remodeling. Conclusion: In adults with obesity, distinct states of NAFLD are associated with intrahepatic perturbations in genes related to inflammation, complement and coagulation pathways, and tissue remodeling. These data provide insights into the dynamic pathogenesis of NAFLD in high-risk individuals.
Indexed as
Identifiers
What OpenQuestion holds
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.