SMAD3 and kidney disorder: They found that disruption of TGF-β-RII inhibited severe tubulointerstitial fibrosis in the unilateral ureteral obstructive (UUO) nephropathy model through the TGF-β/SMAD3 signaling pathway, whereas deletion of TGF-β-RII enhanced renal inflammation in a TGF-β/SMAD3-independent manner [28], alluding to the complex role of TGF-β in renal diseases.