NDUFA7 is an accessory subunit of mitochondrial Complex I (NADH:ubiquinone oxidoreductase) involved in electron transfer from NADH to ubiquinone within the respiratory chain 1. As a non-catalytic component, NDUFA7 facilitates Complex I assembly and function rather than participating directly in catalysis. The gene plays critical roles in cardiac homeostasis and mitochondrial bioenergetics across multiple tissues. Mechanistically, NDUFA7 depletion increases reactive oxygen species (ROS) production and activates calcineurin signaling 1. It can be regulated by upstream factors including the micropeptide MPM, which modulates Complex I activity and NAD+/NADH ratios 2. NDUFA7 expression is also sensitive to circulating immune factors, with B cell-derived miR-3960 delivered via extracellular vesicles reducing NDUFA7 levels and impairing mitochondrial respiratory capacity 3. Clinically, NDUFA7 dysfunction associates with multiple diseases. Decreased cardiac NDUFA7 correlates with pathological cardiac hypertrophy in HCM and DCM 1. Genetic variants aggregate in rheumatoid arthritis with severe erosive disease, implicating ROS dysregulation 4. Reduced NDUFA7 expression appears in COPD and venous thromboembolism with liver cirrhosis [PMID:38181234; 54]. Disrupted NDUFA7 circadian rhythm patterns occur in diabetic stem cells 6, and altered splicing affects oocyte maturation quality 7.