The prevalence of diabetic cardiomyopathy (DCM) increases year by year with the increase in the prevalence of diabetes mellitus (DM), which is one of the most serious cardiovascular complications of DM and a major cause of death in diabetic patients. Although the pathological molecular features of DCM have not been fully elucidated, increasing evidence suggests that impaired autophagy in cardiomyocytes plays a nonnegligible role in the development of DCM. It has been shown that SUMOylation [SUMO = small ubiquitin-like modifier], a post-translational modification of proteins, and its associated ubiquitin-proteasome system mediates protein quality control in the heart and plays an important role in the proteotoxic environment of the heart. Specifically, the expression of ubiquitin-conjugating enzyme E2 (Ubc9), the only SUMO-E2 enzyme, exerts a positive regulatory effect on autophagy in cardiomyocytes with potential cardioprotective effects. This review focuses on the role that autophagy plays in DCM and the potential for Ubc9-regulated autophagy pathways to ameliorate DCM, highlighting the potential of Ubc9 as an interventional target in DCM and providing new insights into the pathogenesis of the disease.

中文翻译：

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泛素结合酶 E2 调节糖尿病心肌病自噬：小综述

随着糖尿病(DM)患病率的增加，糖尿病心肌病(DCM)的患病率逐年上升，是DM最严重的心血管并发症之一，也是糖尿病患者死亡的主要原因。尽管DCM的病理分子特征尚未完全阐明，但越来越多的证据表明心肌细胞自噬受损在DCM的发生发展中起着不可忽视的作用。研究表明，SUMO化[SUMO =小泛素样修饰剂]是蛋白质的翻译后修饰，其相关的泛素-蛋白酶体系统介导心脏中的蛋白质质量控​​制，并在心脏的蛋白毒性环境中发挥重要作用。具体而言，泛素结合酶 E2 (Ubc9)（唯一的 SUMO-E2 酶）的表达对心肌细胞的自噬发挥正向调节作用，具有潜在的心脏保护作用。本综述重点关注自噬在 DCM 中的作用以及 Ubc9 调节的自噬途径改善 DCM 的潜力，强调了 Ubc9 作为 DCM 干预靶点的潜力，并为该疾病的发病机制提供了新的见解。