Thus, changes in the expression of TGF-β1, Smad2/Smad3, αSMA, COL1A1, collagen, and fibronectin in the CKD model reflect excessive ECM accumulation and continuous fibrosis progression, which ultimately lead to structural changes in the renal tissues and functional decline (Eddy, 2005). This evidence concerns the gene ACTA1 and chronic kidney disease.