Myeloid-Specific STAT3 Deletion Aggravates Liver Fibrosis in Mice Fed a Methionine- and Choline-Deficient Diet via Upregulation of Hepatocyte-Derived Lipocalin-2.

ABSTRACT: The signal transducer and activator of transcription 3 (STAT3) in myeloid cells suppresses proinflammatory cytokine production and reduces collagen deposition. However, its role in methionine- and choline-deficient (MCD) diet-fed mice remains unclear. This study investigates the effects of myeloid-specific STAT3 deficiency on hepatic inflammation and fibrosis in MCD diet-fed mice. Myeloid-specific STAT3 knockout (mSTAT3KO) mice were fed the MCD diet for four weeks to induce metabolic dysfunction-associated steatohepatitis (MASH). MCD diet-fed mice displayed MASH-like pathological phenotypes, including hepatic steatosis, inflammation, and fibrosis. Compared with MCD diet-fed WT mice, mSTAT3KO mice fed the MCD diet exhibited reduced hepatic lipid accumulation but increased fibrosis. Notably,

SUBMITTER: Kim KE 

PROVIDER: S-EPMC12524133 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature