TGF-β-driven reduction of CYGB is associated with oxidative DNA damage of HSCs in NASH

This study shows that the molecular regulatory mechanism of TGF-β-induced downregulation of CYGB expression in human HSCs, leading to the loss of cellular tolerance to exogenous oxidative stress and oxidative DNA damage in activated HSCs in human NASH with advanced fibrosis. Our findings provide new insights into the relationship between CYGB expression and the pathophysiology of NASH fibrosis in the human liver.