FDX1-mediated cuproptosis promotes cholestaic liver injury exacerbated by taurocholic acid

As the primary route for copper elimination, cholestasis raises questions about the role of copper in cholestatic liver injury and its specific molecular mechanisms. Our findings reveal that cholestasis-induced copper overload drives liver injury via taurocholic acid (TCA) -exacerbated and FDX1-mediated cuproptosis. Overall design: Mouse AML12 cells cultured in standard growth medium (Group A), or treated with CuCl2 (300 µM)/elesclomol (ES, 40 nM; Group B), or treated with CuCl2 (300 µM)/ES (40 nM)/TCA (1000 µM; Group C), or treated with TCA (1000 µM; Group D) for 24 h (n = 3/group).