Additionally, it has been demonstrated that the major factors involved in the development of glomerulosclerosis and interstitial fibrosis of DN (e.g., TGF-β and angiotensin II) [51, 52] could negatively regulate the receptor-mediated endocytosis [53, 54], participating in enhanced uVDBP excretion. This evidence concerns the gene TGFB1 and liver dysplastic nodule.