In primary mouse cardiomyocytes, hypoxia increased circHIPK3 and promoted its release in exosomes. These cardiomyocyte-derived exosomal circHIPK3 signals to cardiac endothelial cells during myocardial infarction-related angiogenesis.
Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction.