Similarly, miR-29b is lowly expressed in both AngII-induced fibrotic hearts and cardiac fibroblasts, while the over-expression of miR-29b can prevent AngII-induced cardiac fibrosis and cardiac dysfunction by blocking the TGF-β/Smad3 signaling pathway, with the therapeutic potential for hypertensive heart disease (Zhang et al., 2014). This evidence concerns the gene AGT and hypertensive heart disease.