In primary neonatal mouse cardiomyocytes, Ang II treatment induced an in vitro hypertrophy model and increased circHIPK3 expression compared with control cells. circHIPK3 knockdown reduced Ang II-induced cardiomyocyte hypertrophic phenotypes.
Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p.