ArticleWorld journal of gastroenterology2025
FBP1 as a key regulator of focal adhesion kinase-mediated hepatic stellate cell activation: Multi-omics and experimental validation.
Article in World journal of gastroenterology, 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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2 citing papers in PubMed.
- UNC5B activates hepatic stellate cells and promotes liver fibrosis via FAK.Cell communication and signaling : CCS · 2026Article
- Integrative Multiomics Analysis Identifies HK2 as a Key Regulator of Metabolic Reprogramming in Hepatic Stellate Cells.Human mutation · 2025Article
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16 authors.
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Abstract
backgroundInhibiting hepatic stellate cell (HSC) activation is a key therapeutic strategy in liver fibrosis (LF). During activation, aerobic glycolysis is upregulated to meet increased energy demands. Although focal adhesion kinase (FAK) has been implicated in regulating HSC glycolysis, its precise role in activation remains unclear.
aimTo investigate the effects of FAK and fructose-1, 6-bisphosphatase 1 (FBP1) on LF through the modulation of aerobic glycolysis in HSCs.
methodsEighteen mice were randomly assigned to three groups: Control, carbon tetrachloride (CCl₄)-induced LF, and CCl₄ with FAK inhibitor treatment. Liver tissues were analyzed using transcriptomic and proteomic sequencing. Differential gene expression, Mfuzz clustering, and protein interaction network analyses identified key regulatory factors. Immunohistochemistry (IHC) and Western blot (WB) analysis were used to assess FAK and FBP1 expression, along with glycolysis-related enzymes. The migratory behavior of HSCs was evaluated using Transwell migration and scratch assays.
resultsTranscriptomic and proteomic analyses revealed significantly reduced FBP1 expression in CCl₄-induced fibrosis, which was restored upon FAK inhibition. Histological staining (hematoxylin and eosin, Masson's trichrome, Sirius red) confirmed reduced fibrosis following FAK inhibition. WB analysis demonstrated suppression of glycolysis-related enzymes. In LX-2 cells, FAK inhibition attenuated HSC activation and glycolysis while upregulating FBP1. Exogenous recombinant FBP1 inhibited HSC activation and glycolysis. Transwell and scratch assays showed that FBP1 significantly impaired HSC migration. In addition, WB and IHC analyses confirmed lower FBP1 expression in fibrotic liver tissues from patients compared to healthy controls.
conclusionFAK inhibitors and increased FBP1 expression inhibit aerobic glycolysis in HSCs, thereby improving LF. Thus, FAK and FBP1 may be potential targets for LF treatment.
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