Mcu upregulation triggers mitochondrial oxidative stress and cardiomyocyte injury after myocardial infarction yet is suppressed by Fto and Ythdf2 in an m6A-dependent manner.
It is demonstrated that elevated Mcu is positively associated with MI risk; excess Mcu triggers mitochondrial calcium overload, ROS buildup, mitochondrial membrane potential loss and respiratory chain damage to facilitate cardiomyocyte damage, whereas Mcu knockdown alleviate these pathological alterations.