糖尿病视网膜病变(DR)是糖尿病患者常见且严重的微血管并发症之一，已成为全球致盲的主要原因之一。随着糖尿病患病率持续上升，深入探究DR的发病机制及其有效干预手段具有重要的临床意义。雷帕霉素靶蛋白(mTOR)作为一种蛋白激酶，广泛参与细胞生长、代谢和自噬等过程。研究表明，mTOR信号通路在DR病理进程中发挥重要调控作用，其活性异常可导致视网膜细胞自噬功能紊乱，从而加速细胞损伤与疾病发展。自噬作为细胞稳态的重要调节机制，通过清除受损细胞器和蛋白质聚集，维持细胞功能平衡。文章系统综述了mTOR信号通路的结构功能、自噬的分子调控机制及其在视网膜病理变化中的作用，通过归纳当前的研究成果，旨在明确mTOR-自噬轴在DR中的关键调控作用，为揭示DR的分子发病机制提供理论支撑，并为开发新型靶向治疗策略提供潜在靶点和研究方向，具有重要的科学意义和临床价值

Diabetic retinopathy(DR)is one of the most common and severe microvascular complications in diabetic patients and has become one of the leading causes of blindness worldwide. With the continuous rise in the prevalence of diabetes, in-depth exploration of the pathogenesis of DR and effective intervention measures is of great clinical significance. The mechanistic target of rapamycin(mTOR), as a protein kinase, is widely involved in cellular processes such as growth, metabolism, and autophagy. Research indicates that the mTOR signaling pathway plays a crucial regulatory role in the pathological progression of DR, and its abnormal activity can disrupt retinal cell autophagy function, thereby accelerating cellular damage and disease progression. Autophagy, as an important regulatory mechanism for cellular homeostasis, maintains cellular functional balance by clearing damaged organelles and protein aggregates. This article provides a systematic review of the structural and functional aspects of the mTOR signaling pathway, the molecular regulatory mechanisms of autophagy, and their roles in retinal pathological changes. By summarizing current research findings, the article aims to clarify the key regulatory role of the mTOR-autophagy axis in DR, providing theoretical support for elucidating the molecular pathogenesis of DR and offering potential targets and research directions for developing novel targeted therapeutic strategies, thereby holding significant scientific and clinical value.

河南省医学科技攻关计划省部共建重点项目(No. SBGJ202402093); 中原科技领军人才项目(No. 224200510013)