The increased TGF-β1 stimulates EMT, EndMT and ECM formation, which induce renal fibrosis, glomerular endothelial damage, glomerular sclerosis and podocyte injury, and the increased osteopontin changes the phenotype of MCs from contractile to synthetic, which induces MC proliferation in the pathogenesis of diabetic nephropathy. Here, SPP1 is linked to glomerulosclerosis.