Sp1 regulation of TGF-β involvement in fibrosis was further supported by the findings that the up-regulation of the Sp1/ TGF-β pathway may be one mechanism, by which the deletion of Smad7 enhanced hypertensive cardiac remodeling, which suggests that Sp1 may be a crucial mediator of cardiac fibrosis and remodeling [10]. Here, SMAD7 is linked to fibrosis.