KLF15 and cardiac hypertrophy: It was proved that miR-223-3p in cultured cardiomyocytes was increased under 1% O2 hypoxia and directly suppressed Kruppel-like factor 15 (KLF15), a regulator of cardiomyocyte structure and function to repress cardiac hypertrophy, to promote hypoxia-induced apoptosis and oxidative stress of cardiomyocytes (82), although others reported that 10% O2 alveolar hypoxia induced reduction of miR-223-3p expression in ventricular myocardium of mice (84).