FNDC3B and myocardial infarction: Studies has reported that circSRY confers protection to hypoxic cardiomyocytes by reducing apoptosis through repression of miR‐13822; circ‐HRCR was located in cytoplasm, and served as miR‐223 sponge to upregulate ARC expression in cardiac hypertrophy22; circ‐FOXO3 was located in cytoplasm, and accelerated cardiac senescence through interacting with protein ID‐1 and transcription factor E2F123; circ‐Fndc3b regulated myocardial infarction by binding with protein FUS to modulate VEGF level.24