PPARGC1A and acute kidney injury: The expression of PGC-1α is markedly suppressed during AKI induced by folic acid (FA), ischemia/reperfusion, or glycerol, while overexpression of PGC-1α in tubular epithelial cells can restore mitochondrial and cellular function and decrease epithelial–mesenchymal transition after oxidative stress (Rasbach and Schnellmann, 2007; Hallman et al., 2008; Yuan et al., 2012), suggesting that PGC-1α may play a pivotal role in the recovery after AKI and in the fibrotic response.