NDUFA11 is an accessory subunit of mitochondrial Complex I (NADH dehydrogenase), a key enzyme complex in cellular respiration that transfers electrons from NADH to ubiquinone in the respiratory chain 1. As a non-catalytic component, NDUFA11 plays a structural or regulatory role in Complex I assembly and function rather than direct catalysis 2. Clinically, NDUFA11 dysregulation is associated with multiple disease states. Anti-NDUFA11 autoantibodies were detected in 3.5% of inclusion body myositis (IBM) patients, showing higher frequency than in polymyositis or dermatomyositis, and correlating with a trend toward distal lower extremity weakness and elevated creatine kinase levels 1. In acute myocardial infarction, NDUFA11 expression is significantly reduced and serves as a protective biomarker against major adverse cardiovascular events, with diagnostic value (AUC > 0.85) 2. NDUFA11 has also been identified as a hub gene in disulfidptosis-related signatures for epilepsy, cervical cancer, and bladder cancer, where it associates with altered Complex I assembly and cell death pathways 345. Additionally, environmental toxins may disrupt mitochondrial function through NDUFA11 interaction, triggering oxidative stress 6. These findings establish NDUFA11 as a critical mediator of mitochondrial bioenergetics with emerging roles as a disease biomarker across inflammatory, cardiovascular, and malignant conditions.