ArticleActa pharmaceutica Sinica. B2024
FGF4 protects the liver from immune-mediated injury by activating CaMKK
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed.
- The role of FGF19-FGFR4 signaling pathway in liver health and disease: Guardian or destroyer.Genes & diseases · 2026Review
- Lipocalin 13 Mitigates Metabolic Dysfunction-Associated Steatotic Liver Disease Through Inhibiting the ADRB2/ERK Signalling Pathway.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- FGF family in health and disease.Molecular biomedicine · 2026Review
- Ferroptosis regulatory networks and precision interventions in autoimmune hepatitis: comparison with cholestatic diseases.Frontiers in immunology · 2026Review
- HNF4A ameliorates acute liver failure by inhibiting NCOA4-mediated ferritinophagy.Scientific reports · 2025Article
- Protective Effect of Hordenine on Concanavalin A-Induced Hepatic Injury.Journal of inflammation research · 2025Article
- Fibroblast growth factor signaling in macrophage polarization: impact on health and diseases.Frontiers in immunology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune-mediated liver injury (ILI) is a condition where an aberrant immune response due to various triggers causes the destruction of hepatocytes. Fibroblast growth factor 4 (FGF4) was recently identified as a hepatoprotective cytokine; however, its role in ILI remains unclear. In patients with autoimmune hepatitis (type of ILI) and mouse models of concanavalin A (ConA)- or S-100-induced ILI, we observed a biphasic pattern in hepatic FGF4 expression, characterized by an initial increase followed by a return to basal levels. Hepatic FGF4 deficiency activated the mitochondria-associated intrinsic apoptotic pathway, aggravating hepatocellular apoptosis. This led to intrahepatic immune hyper-reactivity, inflammation accentuation, and subsequent liver injury in both ILI models. Conversely, administration of recombinant FGF4 reduced hepatocellular apoptosis and rectified immune imbalance, thereby mitigating liver damage. The beneficial effects of FGF4 were mediated by hepatocellular FGF receptor 4, which activated the Ca
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