ArticleScience advances2024
Compromised macrophages contribute to progression of MASH to hepatocellular carcinoma in FGF21KO mice.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- A refined MASH-HCC model identifies macrophage Gadd45b as a key orchestrator of inflammation-driven neoplastic progression.Experimental & molecular medicine · 2026Article
- Hepatoma-Derived Growth Factor Coordinates STAT3 Pathway and Exosome-Mediated Intrahepatic Crosstalk to Control Hepatic Steatosis and MASLD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-omics integration model of exosome metabolomics and PD-1/PD-L1 expression for early prediction of immunotherapy efficacy in advanced liver cancer.Scientific reports · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- FGF21 promotes the resolution of inflammation through the ALOX15/SPM pathway in acute respiratory distress syndrome.Respiratory research · 2026Article
- Sexual Dimorphism in the Initial Apoptotic Switch During MASH Progression in Mice.International journal of molecular sciences · 2026Article
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- Decoding the CHI3L1/IL-13Rα2 signaling nexus in MASH-fibrosis pathogenesis.Science advances · 2025Article
- Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.Cellular & molecular immunology · 2025Review
- Sphingosine 1-phosphate derived from tumor-educated hepatic stellate cells combining with S1PR4 promotes tumor associated macrophages differentiation through FAO modulation.Scientific reports · 2025Article
- FGF21 inhibits invasion and metastasis via IL-17A-Notch in pancreatic ductal adenocarcinoma.Frontiers in oncology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Metabolic dysfunction-associated steatohepatitis is well accepted as a potential precursor of hepatocellular carcinoma. Previously, we reported that fibroblast growth factor 21 (FGF21) revealed a novel anti-inflammatory activity via inhibiting the TLR4-IL-17A signaling, which could be a potential anticarcinogenetic mechanism to prevent to MASH-HCC transition. Here, we set out to determine whether FGF21 has a major impact on Kupffer cells' (KCs) ability during MASH-HCC transition. We found aberrant hepatic FGF21 and KC pool in human MASH-HCC. Lack of FGF21 up-regulated ALOX15, which converted the oxidized fatty acids to induce excessive KC death and mobilization of monocyte-derived macrophages (MoMFs) for KC replacement. Lack of FGF21 oversupplied free fatty acids for sphingosine-1-phosphate (S1P) cascade synthesis to mediate MASH-HCC transition via S1P-YAP signaling and cross-talk between tumor cells and macrophages. In conclusion, lack of FGF21 accelerated MASH-HCC transition via the S1P-YAP signaling. Compromised MoMFs could present as tumor-associated macrophage phenotype rendering tumor immune microenvironment for MASH-HCC transition.
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