Fig. 6

Influences of miR-325-3p dysregulation on the viability of cardiomyocytes in vitro. a Both the up- and downregulation of miR-325-3p affect the cell viability of hypoxia-induced cardiomyocytes. b The protein expression of RIPK1, RIPK3 and p-MLKL in cardiomyocytes is shown. Representative images (top) and quantitative comparisons (bottom) are shown. **P < 0.01 compared to cells cultured under normal conditions, ^##P < 0.01 compared to cells treated with hypoxia + agomiR-control + Z-IETD-FMK. MI, myocardial infarction; agomiR-325-3p, miR-325-3p agomir; antagomiR-325-3p, miR-325-3p antagomir; agomiR-control, scrambled agomir or antagomir control; Z-IETD-FMK, a caspase inhibitor, benzyloxycarbonyl (Cbz)-Ile-Glu (OMe)-Thr-Asp (OMe)-FMK; RIPK1, receptor-interacting serine/threonine protein kinase 1; RIPK3, receptor-interacting serine/threonine protein kinase 3; p-MLKL, phosphorylated mixed-lineage kinase domain-like protein