Prevention of spontaneous hepatocarcinogenesis in farnesoid X receptor–null mice by intestinal‐specific farnesoid X receptor reactivation

Abstract

Intestinal FXR is sufficient to restore BA homeostasis through the FGF15 axis and prevent progression of liver damage to HCC even in the absence of hepatic FXR. Intestinal-selective FXR modulators could stand as potential therapeutic intervention to prevent this devastating hepatic malignancy, even if carrying a somatic FXR mutation.