Hepatocyte FoxO1 Deficiency Protects from Liver Fibrosis via Reducing Inflammation and TGF-β1 Mediated HSC Activation

Liver fibrosis was established by carbon tetrachloride (CCL4) administration and compared between liver-specific deletion of FoxO1 deletion (F1KO) and control (CNTR) mice. Using genetic and bioinformatic strategies in vitro and in vivo, the role of hepatic FoxO1 in liver fibrosis and associated mechanisms was established.