In the present study, Ang II was found to induce myocardial hypertrophy, fibrosis, oxidative stress, and inflammation, as evidenced by alterations in the PI3K/AKT1/mTOR/ERK, TGF-β/Smad2/3, NF-κB, and NOX1 signaling pathways (Fig. 6). This evidence concerns the gene NOX1 and cardiac hypertrophy.