At least 3 possible explanations to support this idea: first, AGEs may cross-link with type IV collagen, elastin to increase ventricular stiffness; second, AGEs may impair myocardial calcium handling and lead to diastolic dysfunction [33]; third, AGEs may stimulate the excretion of TGF-β, thus increasing the ECM [9], and myocardial fibrosis. This evidence concerns the gene TGFB1 and Myocardial fibrosis.