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. 2020 Jul 21;42(4):499–507. doi: 10.1038/s41401-020-0471-x

Fig. 1. NcRNAs involved in different mechanisms of DOX-induced cardiac cell apoptosis.

Fig. 1

MiR-499-5p and miR-532-3p regulate DOX-induced mitochondrial fission; miR-15b-5p, miR-23a, miR-29b, miR-146a and LincRNA-p21 regulate the DOX-induced decline in mitochondrial membrane potential and cytochrome c release; miR-15b-5p, miR-23a, miR-30 and LincRNA-p21 regulate DOX-induced ROS production; miR-140-5p, miR-451 and LincRNA-p21 regulate DOX-induced change of antioxidant levels; miR-378 regulates DOX-induced ER stress; miR-320a regulates the DOX-induced impact on microvessel density; miR-21, miR-34a-5p, miR-130a, miR-208a, miR-212/132, Linc00339, LncRNA CHRF, LncRNA Mhrt and CircRNA derived from the Ttn 105-111 gene regulate DOX-induced apoptosis with no clearly indicated mechanisms; and LncRNA FOXC2-AS1 regulates DOX-induced reduction in cell viability.