[关键词]
[摘要]
糖尿病视网膜病变(DR)是糖尿病主要微血管并发症，其病理机制与高血糖诱导的氧化应激、慢性炎症及神经元损伤密切相关。蛋白翻译后修饰(PTM)通过动态调控蛋白质功能，在DR发生发展中起关键作用。磷酸化、乙酰化、泛素化及O-糖基化等PTM通过影响血管通透性、炎症因子释放、细胞存活及代谢紊乱，协同驱动DR的微血管病变与神经退行性改变。不同PTM间的复杂交互作用揭示了疾病的多维度病理特征。未来需深入解析PTM动态调控网络，开发靶向特异性修饰的干预策略，并整合前沿技术探索其在视网膜细胞异质性中的作用，为DR的精准治疗提供新方向。
[Key word]
[Abstract]
Diabetic retinopathy(DR), a major microvascular complication of diabetes, is driven by hyperglycemia-induced oxidative stress, chronic inflammation, and neurodegeneration. Post-translational modifications(PTM)play pivotal roles in DR progression by dynamically regulating protein functions. Key PTMs, including phosphorylation, acetylation, ubiquitination, and O-glcNAcylation, collectively exacerbate vascular dysfunction, inflammatory responses, metabolic dysregulation, and neuronal damage. The intricate crosstalk among PTM underscores the multifaceted pathology of DR. Future research should focus on elucidating PTM interaction networks, developing targeted modulators, and leveraging advanced technologies to uncover their roles in retinal cellular heterogeneity, thereby advancing precision therapeutic strategies for DR.
[中图分类号]
[基金项目]
无锡市“双百”中青年医疗卫生拔尖人才项目(No.BJ2023036)
