Our study revealed that Glce deficiency in renal tubular cells promoted TGF‐β/Smad pathway activation predominantly associated with TGFBR1 rather than Smad3, however, inhibition of TGF‐β/Smad pathways partially relieved renal fibrosis in Glce‐/‐ mice after UUO. This evidence concerns the gene SMAD3 and renal fibrosis.