In primary mouse cardiac endothelial cells exposed to oxidative stress, exosome pretreatment increased circHIPK3 levels, with hypoxic cardiomyocyte-derived exosomes producing higher circHIPK3 expression than normoxic exosomes.
Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction.