In the model of cardiomyopathy induced by Dox, overexpressed circ-Foxo3 can interact with the anti-senescent protein ID-1, transcription factor E2F1 and the anti-stress proteins FAK, HIF1α, which are in turn restricted to be translocated to the nucleus to exert their functions, leading to cardiac senescence and apoptosis; whereas silencing endogenous circ-Foxo3 inhibits senescence and relieves cardiomyopathy [90]. This evidence concerns the gene FOXO3 and cardiomyopathy.