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Background Circular RNA (circRNA) has been shown to play an important role in a variety of cardiovascular diseases, including myocardial infarction (MI). However, the role of  circRbms1  in MI progression remains unclear. Methods An MI mouse model was constructed in vivo, and cardiomyocytes were cultured under hypoxia condition to induce a cardiomyocyte injury model in vitro. The expression levels of  circRbms1 , microRNA ( miR)-742-3p , and forkhead box O1 ( FOXO1 ) were determined by quantitative real-time PCR. Cell viability, migration, invasion, and apoptosis were measured using Cell Counting Kit-8 assay, transwell assay, and flow cytometry. Meanwhile, western blot analysis was used to examine the protein levels of apoptosis markers and FOXO1. Additionally, dual-luciferase reporter assay, RNA pull-down assay, and RIP assay were employed to verify the interactions between  miR-742-3p  and  circRbms1  or  FOXO1 . Results CircRbms1  was upregulated in the heart tissues of MI mice and hypoxia-induced cardiomyocytes. Hypoxia induced cardiomyocyte injury by suppressing cell viability, migration, and invasion, and promoting apoptosis. Function experiments showed that  circRbms1  overexpression aggravated hypoxia-induced cardiomyocyte injury, while its silencing relieved cardiomyocyte injury induced by hypoxia. Furthermore,  circRbms1  sponged  miR-742-3p .  MiR-742-3p  overexpression alleviated hypoxia-induced cardiomyocyte injury, and its inhibitor reversed the suppressive effect of  circRbms1  silencing on hypoxia-induced cardiomyocyte injury. Further experiments showed that  FOXO1  was a target of  miR-742-3p , and its expression was positively regulated by  circRbms1 . The inhibitory effect of  miR-742-3p  on hypoxia-induced cardiomyocyte injury was reversed by FOXO1 overexpression. Conclusion CircRbms1  regulated the  miR-742-3p / FOXO1  axis to mediate hypoxia-induced cardiomyocyte injury, suggesting that  circRbms1  might be an effective target for MI treatment.

CircRbms1 knockdown alleviates hypoxia-induced cardiomyocyte injury via regulating the miR-742-3p/FOXO1 axis