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Hepatocyte FoxO1 depletion exacerbates hepatic inflammation in MASH

GSE293003 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/07/30 Platform GPL34284
Summary
The transcription factor Forkhead box protein O1 (FoxO1) is a well-established regulator of glucose and lipid metabolism, yet its role in metabolic dysfunction-associated steatohepatitis (MASH) pathogenesis remains debated. This study investigates hepatocyte-specific FoxO1 mechanisms driving hepatic inflammation in MASH. Using hepatocyte-specific FoxO1-knockout (KO) mice fed a methionine-choline-deficient diet and LPS-treated FoxO1-KO cells, we demonstrate FoxO1 depletion exacerbates hepatic inflammation, ballooning degeneration, and upregulates TNF-alpha, CXCL8, and CXCL2 in vivo and in vitro. Transcriptomics linked FoxO1 deficiency to enriched pro-inflammatory pathways and suppressed cysteine/methionine metabolism.
Published in
Hepatocyte FoxO1 depletion exacerbates hepatic inflammation in MASH by targeting cystathionine γ-lyase
Chen HT, Huang C, Chen JW et al. · Scientific reports 2025 · PMID 40695937 · doi:10.1038/s41598-025-10192-x
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Also filed as BioProject PRJNA1242093 and SRA study SRP573159. Searching any of these in the dataset finder brings you back here.

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