Morphological abnormalities and loss of function of mitochondria will lead to increased ROS production and decreased antioxidant GSH and SOD levels, whereas imbalance of oxidative products and antioxidants will lead to the development of oxidative stress, triggering the progression of renal fibrosis (Zhang et al., 2021; Braga et al., 2022). Here, SOD1 is linked to renal fibrosis.