Reduced mitochondrial biogenesis has been previously linked to the fibrotic process in kidney diseases [45,46], and SFN has been shown to prevent it by activating PGC-1α, the main regulator of mitochondrial biogenesis in kidney damage models such as maleate-induced AKI and streptozotocin-induced DN [13,16,33]. Here, PPARGC1A is linked to acute kidney injury.