PPARGC1A and renal fibrosis: As a result, podocyte damage accumulates, leading to elevated levels of albuminuria (Akhtar and Siragy, 2019) (3) Overproduction of ROS triggers the generation of transforming growth factor-beta (TGF-β), suppresses nitric oxide (NO) levels, and leads to renal fibrosis and damage to endothelial cells (Honda et al., 2019) (4) Excessive ROS hinder mechanistic target of rapamycin complex 1 (mTORC1) and AMPK function, affecting PGC-1α activation.