Hepatocellular cystathionine γ lyase/hydrogen sulfide attenuates nonalcoholic fatty liver disease by activating farnesoid X receptor

Abstract

FXR sulfhydration is a post-translational modification affected by hepatic endogenous CSE/H₂ S that may promote FXR activity and attenuate NAFLD. Hepatic CSE deficiency promotes development of nonalcoholic steatohepatitis. The interaction between H₂ S and FXR may be amenable to therapeutic drug treatment in NAFLD.