Diabetic cardiomyopathy (DCM), a lethal cardiovascular complication of diabetes, lacks effective therapies. Regulated in development and DNA damage response 1 (REDD1), a stress-responsive gene implicated in diabetic pathologies, was investigated for its role in autophagy and ferroptosis during DCM progression. Diabetic mice (high-fat diet/streptozotocin-induced) and high glucose (HG)-exposed human AC16 cardiomyocytes were utilized. REDD1 expression was analyzed via RT-qPCR/western blot. Cardiac function, fibrosis (H&E/Masson staining), metabolic parameters (blood glucose, insulin resistance), autophagy (LC3-II/p62, immunofluorescence), and ferroptosis (iron overload, lipid peroxidation, Mito-FerroGreen) were assessed. REDD1 was upregulated in diabetic hearts and HG-treated cardiomyocytes. REDD1 ablation in mice attenuated hyperglycemia, restored cardiac function, reduced hypertrophy/fibrosis, and suppressed autophagy/ferroptosis. In vitro, REDD1 knockdown enhanced cardiomyocyte viability (CCK-8 assay) and mitigated injury (lactate dehydrogenase release). Mechanistically, REDD1 silencing reduced ferroptosis, which was dependent on autophagy inhibition, as both rapamycin (autophagy activator) and Erastin (ferroptosis inducer) partially reversed the protective effects of REDD1 siRNA. These findings identify REDD1 as a critical mediator of DCM via autophagy-driven ferroptosis, offering a novel therapeutic target for diabetic cardiovascular complications.