Transgenic mice with increased circulating levels of TGF-β1 developed glomerulosclerosis and those with increased tubular production of TGF-β1 developed tubulointerstitial fibrosis in the absence of any additional injury.32 Furthermore, the role of Smad3 in renal fibrosis is supported, because genetic inhibition of Smad3 reduced ECM in unilateral ureteral obstruction (UUO).33 Here, TGFB1 is linked to glomerulosclerosis.