In addition, TFAM overexpression in overload-induced heart failure models ameliorates mitochondrial ROS, decreases the expression and activity of the metalloproteinases MMP-2 and MMP9, and upregulates the expression of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) (Kunkel et al., 2019). This evidence concerns the gene TFAM and heart failure.