 The study investigates the effects and mechanisms of cellular oppressor of E1A stimulated Genes 1, CIEG1, on diabetic cardiomyopathy in mice, and finds that CIEG1 deficiency exacerbates cardiac dysfunction, hypertrophy, and fibrosis, while CIEG1 overexpression improves these outcomes by improving autophagy. The study also identifies a new role of CIEG1 in inhibiting L2 protein degradation through F-Box protein 27, FBXO 27.