In addition, miR-143-3p overexpression in AF cardiomyocytes was found to increase cell proliferation and viability, inhibit lipid ROS production and mitochondrial superoxide formation and reduce the intracellular concentrations of total iron and Fe2+ by inhibiting glutamic-oxaloacetic transaminase 1 (GOT1)-mediated oxidative damage and cardiac ferroptosis [112]. This evidence concerns the gene GOT1 and atrial fibrillation.