[关键词]
[摘要]
糖尿病性白内障是糖尿病患者常见的并发症之一，其发病机制复杂，主要涉及氧化应激和糖化应激等多种病理过程。自噬是细胞自我保护的重要机制之一，通过清除和处理受损的细胞器和蛋白质，维持细胞内环境的稳态，从而拮抗高糖环境下氧化应激和糖化应激所致的损伤。近来研究表明，糖化应激与氧化应激之间存在相互作用，这种交互影响可能加剧自噬功能的障碍，进而促进糖尿病性白内障的发生与发展，但具体机制并未完全阐明。文章系统综述了自噬在糖尿病性白内障发病中的调控作用，重点探讨糖化应激与氧化应激交互作用下自噬对疾病进展的影响，以期为糖尿病性白内障的分子诊断和靶向治疗提供新思路。
[Key word]
[Abstract]
Diabetic cataract, a prevalent ocular complication of diabetes mellitus, arises from a complex interplay of pathological mechanisms, with oxidative stress and glycation stress playing central roles. Autophagy, a critical cellular self-protection mechanism, sustains intracellular homeostasis by selectively degrading damaged organelles and misfolded proteins, thereby counteracting the detrimental effects of oxidative and glycation stress under hyperglycemic conditions. Emerging evidence indicates a synergistic interaction between glycation stress and oxidative stress, which may exacerbate autophagic dysfunction and accelerate the onset and progression of diabetic cataract. However, the precise molecular mechanisms underlying this relationship remain incompletely understood. This review systematically examines the regulatory role of autophagy inthe pathogenesis of diabetic cataract, with a particular focus on how autophagic impairment influences disease progression under the combined effects of glycation and oxidative stress. By elucidating these mechanisms, the paper aims to provide novel insights into molecular diagnostic approaches and targeted therapeutic strategies for diabetic cataract.
[中图分类号]
[基金项目]
国家自然科学基金资助项目(No.81670852); 江苏省卫生健康委科研项目(No.M2021084); 南通市科技项目(No.MS22022020)
