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Description
Excess copper is reduced by FDX1 to generate Cu, which drives cell death via two primary mechanisms: (1) Cu-mediated aggregation of lipoylated TCA cycle proteins (e.g., DLAT) and loss of Fe-S clusters, and (2) Cu-induced disruption of the Npl4/p97 protein quality-control system
Pang, W
Their mechanism of action primarily involves the inhibition of inflammatory mediators in the cyclooxygenase (COX) pathway
2024;63(12):e202318783
