SMAD3 and diabetic kidney disease: Blockade of TGF-β/Smad3-mediated renal fibrosis by downregulating TGF-β1 and microRNA-21 expression, thereby restoring the balance of Smad signaling by upregulating an inhibitory Smad7, resulting in a possible underlying mechanism by which CHYS inhibits diabetic nephropathy associated with fibrosis.