Both tachypaced atrial HL-1 cardiomyocytes and left atrial appendages (LAAs) of paroxysmal or persistent AF patients display mitochondrial stress, as evidenced by increased HSP60 and HSP10 expression, decreased ATP production, a loss of the mitochondrial membrane potential, and mitochondrial network fragmentation, resulting in contractile dysfunction and AF progression [24]. This evidence concerns the gene HSPE1 and atrial fibrillation.