TGFB1 and Hyperglycemia: This phenomenon is potentiated via TGF-β released by endothelial cells through AGEs and ROS stimulation; hyperglycemia worsens this scenario through increased expression of TGF-β via Akt decreased activity and increased expression of FoxO1, which enhances expression of α-SMA (alpha-smooth muscle actin), and therefore, more dysfunctional collagen synthesis and extracellular matrix degradation and progression of cardiac fibrosis [21].