SMAD7 and diabetic kidney disease: Our previous study has found that MG132 could depress the activation of NF-κB inflammatory signaling through inhibiting the IκBα sumoylation and ubiquitination, and could inhibit the histone ubiquitination and induce apoptosis in rat glomerular mesangial cells induced by high glucose [13, 20] Renal fibrosis in diabetic nephropathy was induced by activation of the TGF-β signaling pathway, which mediates cell proliferation and differentiation, but whether the proteasome inhibitor could treat diabetic nephropathy by blocking ubiquitin degradation of Smad7 was not reported.