We confirmed previous reports that demonstrated that SMAD3 is an important mediator of glomerulosclerosis and renal interstitial fibrosis.Proteinuria was highly SMAD3 dependent.
BMP7 prevents TGFβ-induced GEC network regression, whereas TGFβ-induced MC nodule formation is prevented by SMAD3 siRNA knockdown or ALK5 inhibitors but not BMP7, and increased phospho-SMAD3 was observed in human glomerulosclerosis.