ArticleHuman mutation2025
Integrative Multiomics Analysis Identifies HK2 as a Key Regulator of Metabolic Reprogramming in Hepatic Stellate Cells.
Article in Human mutation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Therapeutic Targets for Hepatic Fibrosis Driven by Hypoxia-Mediated Hepatic Stellate Cell Activation.Biomolecules · 2026Review
- Integrative Multiomics Analysis Reveals a Cancer Stem Cell-Driven Prognostic Signature and Nominates Belinostat for Targeted Therapy in Hepatocellular Carcinoma.Stem cells international · 2026Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Liver damage caused by chronic liver disease frequently leads to hepatic fibrosis. A pivotal step in the fibrotic process is the activation of hepatic stellate cells (HSCs). Previous studies have suggested that enhanced aerobic glycolysis is closely associated with HSC activation. However, a comprehensive analysis of the relationship between hepatic fibrosis and aerobic glycolysis remains lacking. Methods: RNA sequencing of liver tissue from 30 patients with fibrosis or cirrhosis and 8 healthy controls was conducted as part of a comprehensive multiomics approach to discover differentially expressed genes (DEGs). Weighted gene coexpression network analysis (WGCNA) was conducted to detect gene modules associated with liver fibrosis. Functional analyses, including migration and wound healing, were subsequently performed. Furthermore, a machine learning model predicting fibrosis was constructed based on glycolysis-related gene expression and validated using an independent dataset. Its clinical significance was subsequently explored. Protein expression and localization were further validated via western blotting and immunohistochemistry techniques. Results: The expression of HK2 is notably increased in HSCs and is strongly linked to the advancement of liver fibrosis. Within the constructed machine learning model, the random forest algorithm demonstrated the highest predictive performance for liver fibrosis, achieving an area under the curve (AUC) of 0.889. HK2 expression levels also had a positive correlation with clinical signs of liver damage, such as ALT and AST levels. Knockdown of HK2 in HSCs markedly impaired their migratory capacity and wound healing ability. Conclusions: HK2 is involved in activating HSCs, thus promoting the progression of liver fibrosis. These findings suggest that HK2 holds potential as a therapeutic target for liver fibrosis and as a biomarker for predicting its progression.
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