In primary mouse cardiac microvascular endothelial cells, circHIPK3 was reduced after H2O2-induced oxidative stress compared with control cells, and hypoxia-pretreated cardiomyocyte exosomes rescued its level.
Exosomal circHIPK3 Released from Hypoxia-Pretreated Cardiomyocytes Regulates Oxidative Damage in Cardiac Microvascular Endothelial Cells via the miR-29a/IGF-1 Pathway.