Proteomic analysis was performed on liver tissues from baseline control, iron-overloaded, and DFP-RVT-treated mice to identify differentially expressed proteins and affected pathways. Iron overload resulted in marked downregulation of mitochondrial proteins, particularly components of oxidative phosphorylation and iron-sulfur cluster-associated pathways, including frataxin.
Our findings suggest that frataxin may be a key determinant of mitochondrial integrity and function in the context of hepatic iron overload. The observed frataxin loss in IO mice, likely driven by iron toxicity, contributes to hepatocellular damage. Importantly, DFP-RVT treatment restored frataxin expression, which may account for the recovery of mitochondrial protein levels and overall mitochondrial function
