NDUFC1 (NADH:ubiquinone oxidoreductase subunit C1) is an accessory subunit of mitochondrial respiratory Complex I that facilitates electron transfer from NADH to ubiquinone in the electron transport chain 1. As a non-catalytic component, NDUFC1 supports Complex I function in oxidative phosphorylation (OXPHOS) and ATP synthesis rather than directly catalyzing redox reactions. NDUFC1 expression is activated during cellular differentiation and metabolic transitions. Upon OCT4 depletion in embryonic stem cells, NDUFC1 is among key proteins upregulated to enable OXPHOS machinery activation, shifting cells from glycolysis-dependent metabolism toward oxidative phosphorylation 1. Conversely, NDUFC1 expression decreases in contexts of impaired energy metabolism: it is downregulated in adrenocortical carcinoma relative to adenoma 2, in chr4 tendon injuries 3, and in mammary glands of dairy cows fed low-quality forage 4. Dysregulation of NDUFC1 carries clinical significance in multiple diseases. In adrenocortical carcinoma, miR-483-5p suppresses NDUFC1, reducing oxygen consumption and promoting metabolic shift toward glycolysis 2. In acute ischemic stroke, NDUFC1 was identified as a metabolism-related hub gene with diagnostic accuracy (AUC >0.8) and correlation with immune cell infiltration 5. These findings establish NDUFC1 as a biomarker reflecting mitochondrial function status across pathological conditions.