Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction

Figure 6

A schematic cartoon of the circHIPK3/miR-29g/VEGFA axis in cardiac endothelial cells. CircHIPK3 is upregulated in CMs subjected to hypoxia and released to the extracellular space by exosomes. Subsequently, adjacent cardiac endothelial cells internalize these exosomes, which causes circHIPK3 levels to increase in cardiac endothelial cells. CircHIPK3 could inhibit miR-29a activity and then regulate angiogenesis in cardiac endothelial cells by increasing VEGFA expression.