For this purpose, we investigated the alterations of SOD1 expression, oxidative stress marker, inflammation, fibrosis, and regeneration capacity in cardiotoxin (CTX)-injured tibialis anterior (TA) muscles of two Akita diabetic mouse models with different susceptibility to DN, DN-resistant C57BL/6-Akita and DN-prone KK/Ta-Akita mice, and analyzed the role of SOD1 in regeneration of injured muscle in advanced DN. Here, SOD1 is linked to liver dysplastic nodule.