A mitochondrion-located redox enzyme (PRX-3) tissue-specific knockout mouse model showed impaired antioxidant capacity and exacerbated cardiac dysfunction and oxidative stress during HF.225 Cardiomyocyte-specific SOD2-deficient mice die at ~4 months due to HF and showed mitochondrial architecture alterations, with prominent disruption of cristae and increased vacuole formation.226 Another novel mechanism related to the ROS clearance pathway has also been reported. This evidence concerns the gene SOD2 and hydrops fetalis.