Its mechanism of action may involve inhibition of the activation of the Smads signaling pathway, reducing the phosphorylation of Smad-2 and Smad-3, and enhancing the expression of Smad-7 by decreasing the Ang II-mediated expression of TGF-β1, which in turn reduces the production of ECM and mitigates the degree of renal fibrosis, playing a role in the treatment of hypertensive renal damage. Here, SMAD7 is linked to renal fibrosis.