These results suggested that treatment with Ang IV or FoxO1 inhibitor improved myocardial fibrosis in diabetic mice, and the anti-fibrotic effects of Ang IV were mediated via AT4R. Similarly, Bax/Bcl-2 protein ratio, Cl-caspase3 expression level (Figure 4B, 4F-4G), and TUNEL positive signals in the myocardium (Figure S3D, S3G) were dramatically reduced in the Ang IV and the AS groups versus DM group, and the protective effects of Ang IV were virtually eliminated by the addition of divalinal to Ang IV treatment. This evidence concerns the gene BAX and Myocardial fibrosis.