A global loss of Nox2 limits myocardial ROS production and preserves diastolic function in response to diet-induced obesity [87], doxorubicin treatment [88], and myocardial infarction [89], and mitigates cardiac fibrosis in response to AngII, aldosterone, or pressure overload [41,90,91,92], whereas Nox2 overexpression in endothelial cells promotes cardiac fibrosis, inflammation, and diastolic dysfunction in response to AngII [93]. This evidence concerns the gene CYBB and myocardial infarction.