AGO2 and diabetic cardiomyopathy: The results of our previous study demonstrated that under diabetic stress, the miRNAs targeting mt-Cytb and mitochondrial Ago2 expression are reduced, disrupting electron transport chain complex III (ETCIII) subunit assembly, and leading to excessive ROS production.[7] This exacerbates myocardial stiffness and injury through oxidative stress, mitochondrial dysfunction, inflammatory cascades, and fibroblast activation.[64,65] Nuclear Ago2 also plays a crucial role in diabetic cardiomyopathy.