PRDX4 and cholestasis: In this study using a mouse model of BDL-induced cholestatic liver injury, we demonstrated that the overexpression of hPRDX4 significantly reduced cholestasis-related liver damage and fibrosis and improved the total survival of mice after BDL surgery, suggesting that PRDX4 may play a crucial role in the pathological processes of obstructive cholestatic hepatitis (Figure 8).