In a previous study, it was reported that HO-1 overexpression enhances the biogenesis of mitochondria by increasing the protein expression of NRF1, PGC1α, and TFAM [20], and mitochondrial HO-1 is known to play important roles in regulating total protein turnover in mitochondria and in protecting against diseases, such as hypoxia, neurodegenerative diseases, or sepsis, in which substantially increased mitochondrial ROS generation has been implicated [21]. Here, PPARGC1A is linked to neurodegenerative disease.