FDX1-mediated cuproptosis promotes cholestatic liver injury exacerbated by taurocholic acid-enhanced copper accumulation.

ABSTRACT: Cholestatic liver injury, characterized by direct exposure of hepatocytes to retained bile components with elevated concentrations, represents a common manifestation of various hepatobiliary disorders with persistent threats to long-term patient survival despite existing therapies. 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 single-center retrospective study revealed elevated serum copper levels in subjects with increased gamma-glutamyl transferase compared to controls. Single-cell sequencing of biliary atresia (BA) patients' cholestatic liver specimens demonstrated downregulation of FDX1, a key cuproptosis marker, in BA hepatocytes. Bile duct-ligated rats under hig

SUBMITTER: Guo Y 

PROVIDER: S-EPMC12789603 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature