Genetic insights into biological aging and myasthenia gravis: a Mendelian randomization study of telomere length, epigenetic clocks, and mitochondrial DNA copy number

Our findings demonstrate a bidirectional causality between EOMG and epigenetic aging clocks, which indicates that there is a self-reinforcing pathophysiological cycle. The epigenetic age acceleration is both a driver and a result of the progression of EOMG. The correlation between mtDNA-CN and LOMG suggests that there may be a potential compensatory adaptation mechanism to combat chronic oxidative stress in age-related autoimmunity. These results highlight the complex and subtype-dependent contributions of biological aging to the autoimmune-mediated pathology of MG, and provide key mechanistic insights into the subtype-specific aging in MG.