ArticleHepatology (Baltimore, Md.)2026
The OGT-TFF2 axis mediates intrahepatic crosstalk and MASH pathogenesis.
Article in Hepatology (Baltimore, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- IL-10 attenuates metabolic dysfunction-associated steatotic liver disease via modulation of hepatic responses to lipotoxicity.JCI insight · 2026Article
- The Role of CD4Cells · 2026Review
- Hepatocyte-Derived Apoptotic Bodies as Pathological Intercellular Messengers in the Liver.Biomolecules · 2026Review
- CXCR4 inhibition alleviates prostatic inflammation and pelvic pain via suppressing Th17 cell differentiation and oxidative stress in EAP mice.International journal of biological sciences · 2026Article
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10 authors.
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Abstract
BACKGROUND AND
aimsMetabolic dysfunction-associated fatty liver disease (MASLD) encompasses a spectrum of liver pathologies ranging from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis. The mechanisms governing disease progression, particularly the communication between hepatocytes and non-parenchymal cells, remain poorly understood. In this study, we demonstrate a novel paracrine factor through which O‑GlcNAc transferase (OGT) regulates intercellular crosstalk between hepatocytes and immune cells in MASH development. APPROACH AND
resultsOGT and trefoil factor 2 (TFF2) expression were analyzed in human and mouse livers. The effects of the paracrine factor on inflammation and fibrogenesis were further evaluated in a 3D mouse liver spheroid model of MASH. The GalNAc-modified siRNA targeting the paracrine factor was applied in Gubra-Amylin NASH (GAN) diet-fed mice to determine its therapeutic potential in preventing the MASH progression. Decreased OGT expression during MASLD promotes TFF2 transcription and secretion via forkhead box protein A2 (FOXA2) modulation. In 3D mouse liver spheroids, TFF2 exacerbates MASH-related pathologies. Mechanistically, TFF2 enhances hepatic CD4+ T cell proliferation and Th1/Th17 differentiation through CXC motif chemokine receptor 4 (CXCR4)-signal transducer and activator of transcription 1/3 (STAT1/3) signaling, cooperating with CXC motif chemokine ligand 12 (CXCL12) to amplify inflammation. Hepatocyte-specific Tff2 inhibition using GalNAc-modified siRNA in a diet-induced mouse model ameliorates MASH progression without affecting simple steatosis development.
conclusionsThese results identify an OGT-TFF2 axis that mediates the crosstalk between hepatocytes and CD4 T cells during MASH pathogenesis, revealing a potential therapeutic target for the treatment of chronic liver disease.
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