Fig. 7: A cartoon summarising our findings. | Cell Death & Disease

Fig. 7: A cartoon summarising our findings.

From: Mechanistic insights into the role of FAT10 in modulating NCOA4-mediated ferroptosis in pancreatic acinar cells during acute pancreatitis

Fig. 7

During the progression of AP, FAT10 expression is upregulated. It competes with ubiquitin for binding to NCOA4, thereby antagonising its ubiquitination and forming a stable FAT10-NCOA4 complex that is not degraded via the proteasomal pathway. This results in increased NCOA4 expression, which in turn promotes ferroptosis in pancreatic acinar cells. Silibinin, by targeting and inhibiting the FAT10-NCOA4 pathway, can suppress ferroptosis in pancreatic acinar cells.

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