EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes

• EEPD1 deficiency exacerbates radiation-induced cardiac hypertrophy and apoptosis, while overexpression is protective. • EEPD1 directly interacts with FOXO3A and promotes its deubiquitination, leading to FOXO3A degradation. • FOXO3A inhibition reverses the detrimental effects of EEPD1 knockdown, confirming the EEPD1-FOXO3A axis as a key pathway. • This study identifies EEPD1 as a potential therapeutic target for mitigating radiation-induced heart disease.