ArticleFrontiers in immunology2020
Predicting Non-Alcoholic Fatty Liver Disease Progression and Immune Deregulations by Specific Gene Expression Patterns.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- TRIM29-dependent AKR1B10 degradation ameliorates MASH.Science advances · 2026Article
- Immune microenvironment in hepatocellular carcinoma: from pathogenesis to immunotherapy.Cellular & molecular immunology · 2025Review
- Unveiling the role of IL7R in metabolism-associated fatty liver disease leading to hepatocellular carcinoma through transcriptomic and machine learning approaches.Discover oncology · 2025Article
- Bioinformatic analysis of molecular expression patterns during the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD).Scientific reports · 2025Article
- Examination of the causal role of immune cells in non-alcoholic fatty liver disease by a bidirectional Mendelian randomization study.Open medicine (Warsaw, Poland) · 2025Article
- Recent advances in non-alcoholic steatohepatitis-associated hepatocellular carcinoma: immune cells, metabolic dysregulation, and therapeutic strategies.Frontiers in oncology · 2025Review
- Development of a Novel four-gene Model for Monitoring the Progression from Metabolic Dysfunction-associated Steatotic Liver Disease to Hepatocellular Carcinoma in Males.Journal of Cancer · 2025Article
- Single-Cell and Bulk Transcriptomics Reveal the Immunosenescence Signature for Prognosis and Immunotherapy in Lung Cancer.Cancers · 2024Article
- Development of a novel diagnostic model to monitor the progression of metabolic dysfunction-associated steatotic liver disease to hepatocellular carcinoma in females.Discover oncology · 2024Article
- Immune landscape of hepatocellular carcinoma tumor microenvironment identifies a prognostic relevant model.Heliyon · 2024Article
- The pan-cancer landscape of aldo-keto reductase1B10 reveals that its expression is diminished in gastric cancer.Frontiers in immunology · 2024Article
- AKR1B10 and digestive tumors development: a review.Frontiers in immunology · 2024Review
- Article
- Identification of LBH and SPP1 involved in hepatic stellate cell activation during liver fibrogenesis.Human cell · 2023Article
- HNRNPC suppresses tumor immune microenvironment by activating Treg cells promoting the progression of prostate cancer.Cancer science · 2023Article
- CD24 Gene Expression as a Risk Factor for Non-Alcoholic Fatty Liver Disease.Diagnostics (Basel, Switzerland) · 2023Article
- Significance of MiRNA-34a and MiRNA-192 as a risk factor for nonalcoholic fatty liver disease.Journal, genetic engineering & biotechnology · 2023Article
- The ameliorating effect of withaferin A on high-fat diet-induced non-alcoholic fatty liver disease by acting as an LXR/FXR dual receptor activator.Frontiers in pharmacology · 2023Article
- LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis.Cell death discovery · 2022Article
- THC and CBD affect metabolic syndrome parameters including microbiome in mice fed high fat-cholesterol diet.Journal of cannabis research · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide with rising rates in parallel to obesity, type 2 diabetes, and metabolic syndrome. NAFLD includes pathologies ranging from simple steatosis (NAFL) to non-alcoholic steatohepatitis and cirrhosis (NASH), which may eventually develop into hepatocellular carcinoma (HCC). Mechanically, lipids accumulation and insulin resistance act as the first hit, inflammation and fibrosis serve as the second hit. Currently, the diagnosis of NAFLD mainly depends on pathology examination and medical imaging, whereas proper gene signature classifiers are necessary for the evaluation of disease status. Here, we developed three signature classifiers to distinguish different NAFLD disease states (NAFL and NASH). Moreover, we found that B cells, DCs, and MAIT cells are key deregulated immune cells in NAFLD, which are associated with NAFLD and NAFLD-HCC progression. Meanwhile, AKR1B10 and SPP1 are closely related to the above three immune cell infiltrations and immunosuppressive cytokines expressions in NAFLD and NAFLD-HCC. Subsequently, we screened out AKR1B10 and SPP1 sensitive molecules TGX-221, which may provide a possible therapy for NAFLD and NAFLD-HCC.
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