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Ferredoxin 1 (FDX1) is a mitochondrial iron–sulfur protein that functions as an electron carrier, transferring electrons from ferredoxin reductase (FDXR) to various mitochondrial enzymes[1][3]. It contains a [2Fe-2S] iron–sulfur cluster, is highly conserved, and plays major roles in steroid hormone synthesis, bile acid and vitamin D metabolism, TCA cycle enzyme lipoylation, and iron–sulfur cluster biogenesis[1][3][6]. FDX1 is vital for lipid homeostasis and embryonic development; knockout in mice causes embryonic lethality and metabolic disorders, while partial loss leads to lipid accumulation and liver disease but not spontaneous tumors[1]. FDX1 also participates in the regulation of cuproptosis, a form of copper-dependent cell death[1]. It does not act as a direct drug target in current therapeutics, but its role in essential metabolic pathways and disease phenotypes makes it a protein of interest for future drug discovery and biomarker studies[1][3].
Electron transfer to mitochondrial cytochrome P450 enzymes for steroid, bile acid, and vitamin D synthesis Support of iron–sulfur cluster assembly enzymes
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