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IGFBP-7 transforms hepatic stellate cells into an HCC-promoting phenotype in MASLD.

ABSTRACT: Hepatic fibrosis is the strongest contributor to hepatocarcinogenesis in metabolic dysfunction-associated steatotic liver disease (MASLD); however, the underlying mechanisms have yet to be fully elucidated. In 94 human MASLD biopsy samples, artificial intelligence-based morphological phenotyping of hepatic fiber and multi-omics analyses revealed that insulin growth factor-binding protein 7 (IGFBP-7) secreted from senescent periportal endothelial cells might transform stellate cells into a hepatocarcinogenesis-promoting phenotype. To test the effect of IGFBP-7 on HSC, a hepatic stellate cell line, LX-2, was cultured with recombinant IGFBP-7 (100ng/mL), resulting in their transformation to a more activated form than the control.

ORGANISM(S): Homo sapiens

PROVIDER: GSE278593 | GEO | 2025/08/20

REPOSITORIES: GEO

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Spatial single-cell transcriptomics of MASLD-affected liver biopsy samples.

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) liver biopsies were analyzed using spatial single-cell transcriptomics (CosMx Spatial Molecular Imager, NanoString) to elucidate molecular alterations associated with hepatic fibrosis morphology, as quantified by the artificial intelligence-based FibroNest algorithm (PharmaNest). This analysis identified distinct morphological fiber phenotypes (FibroPCs), among which FibroPC4, characterized by reticular fiber structures, was associated with a hepatic stellate cell (HSC) phenotype that promotes hepatocellular carcinoma (HCC). This HCC-promoting HSC phenotype was driven by insulin-like growth factor-binding protein 7 (IGFBP-7) secreted from senescent periportal endothelial cells.

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Project description:Uric acid has garnered increasing attention for its association with metabolic dysfunction-associated steatotic liver disease (MASLD) in recent cross-sectional studies, although detailed understanding of its involvement remains limited. This study confirms a strong association between urate levels and elevated risk of both MASLD and type 2 diabetes (T2D) through a large-scale observational analysis of UK Biobank data. However, Mendelian randomization (MR) analysis involving over 2 million samples identified only causal effects of urate on serum triglyceride levels and the risk of T2D. Additionally, a targeted metabolomics study involving elderly Chinese participants revealed that, rather than UA, allantoin—a byproduct of UA oxidation—was significantly elevated in individuals with dyslipidemia or T2D. Notably, a significant negative correlation was found between serum allantoin level and fasting glucose, as well as serum triglyceride and cholesterol levels. Animal studies demonstrated that allantoin exacerbates hepatic lipid accumulation and glucose intolerance in mice fed a high-fat diet, which was accompanied by increased hepatic lipid biogenesis and reduced bile acid production. Interestingly, our findings indicate that allantoin exhibits a strong binding affinity for PPARα, suggesting that it may act as an inhibitor of PPARα, thereby promoting the progression of MASLD. These results underscore the critical role of allantoin, rather than UA, in the development of MASLD, offering valuable insights for the prediction and management of hepatic metabolic disorders.

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