Ndufa10 encodes a protein with NADH dehydrogenase and oxidoreductase activities in the mitochondrial electron transport chain. It is an accessory subunit of mitochondrial complex I, playing a crucial role in maintaining the integrity and function of this complex, thus being essential for mitochondrial oxidative phosphorylation [3].

In a study on diabetic cardiomyopathy, CAV3 overexpression restored mitochondrial function and alleviated the disease partially through NDUFA10. CAV3 interacted with NDUFA10, reduced its lysosomal degradation, restored complex I activity [1].

In NASH research, AGK deficiency-induced liver damage was attributed to hepatic mitochondrial dysfunction as AGK interacted with NDUFA10 to regulate mitochondrial fatty acid metabolism and maintain complex I function [2].

In Alzheimer's disease, lower NDUFA10 expression levels correlated with a higher degree of dementia. The hypothesis was that reduced METTL3 expression decreased the m6A modification level of NDUFA10 mRNA, reducing its protein expression and contributing to complex I assembly disorder [3].

Also, most mitochondrial dGTP binds tightly to NDUFA10 through its deoxyribonucleoside kinase domain, which may regulate mitochondrial dNTP availability [4].

Mutations in Ndufa10 were found to cause complex I deficiency in a patient with Leigh disease, leading to decreased complex I amount, activity, and disturbed assembly [5].

In a Parkinson's cell model, neuroglobin protected cells against apoptosis by interacting with NDUFA10, rescuing complex I activity [6].

Benzo[a]pyrene inhibited testosterone biosynthesis via NDUFA10-mediated mitochondrial impairment in mouse Leydig cells [7].

And knockout of Ndufa10 in CD8+ T cells led to enhanced tumor growth and increased exhaustion of tumor-infiltrating CD8+ T cells [8].

In conclusion, Ndufa10 is essential for mitochondrial complex I function and mitochondrial oxidative phosphorylation. Studies using various models, including gene knockout in CD8+ T cells, have revealed its significance in multiple disease conditions such as diabetic cardiomyopathy, NASH, Alzheimer's disease, Leigh disease, Parkinson's disease, male steroidogenesis disorder, and cancer-related immune dysfunction. These findings provide insights into potential therapeutic targets for these diseases.