Figure 1.

Prolonged hyperglycemia can produce reactive oxygen species (ROS) via activation of protein kinase C (PKC) pathways and advanced glycation end products (AGEs) production, leading to altered metabolism regulation, altered mitochondrial biogenesis, impaired mitochondrial calcium handling, and impaired electron transport chain. These actions will cause mitochondrial to deteriorate and generate more ROS. The ROS produced results in oxidative stress, which can initiate inflammation, fibrosis, and apoptosis, causing diabetic cardiomyopathy (DCM).