In vascular smooth muscle cells and cardiomyocytes ontogenically related to VSMCs, high NOX4 expression induced by ER stress reduced cell death but promoted cell proliferation, leading to arterial remodeling and myocardial hypertrophy, and exacerbated the deterioration of cardiac function (Mittal et al., 2007; Kuroda et al., 2010). This evidence concerns the gene NOX4 and cardiac hypertrophy.