糖尿病视网膜病变(DR)作为糖尿病主要的微血管并发症，其发生发展与全身及局部代谢紊乱密切相关。酮体代谢在DR发生发展中发挥着重要作用。既往研究发现脂代谢紊乱与DR发展密切相关，酮体作为糖代谢受阻时，脂肪分解的代谢产物，其主要包括β-羟丁酸、乙酰乙酸和丙酮。研究发现，酮体代谢与DR的多个病理生理过程密切相关，如视网膜细胞的氧化应激、炎症反应和神经细胞变性等。文章聚焦酮体代谢在DR发病机制中的调控作用，系统梳理酮体通过代谢重编程、表观遗传修饰及细胞信号转导等途径影响视网膜血管屏障破坏、神经胶质细胞活化及血管新生等核心病理环节的最新研究进展，为深入理解DR的代谢驱动机制提供理论依据。

Ketone body metabolism plays a significant role in the development and progression of diabetic retinopathy(DR), which closely related to the system and local metabolic disorders as a major microvascular complication of diabetes mellitus. Previous research has established a close relationship between dyslipidemia and DR progression. Ketone bodies, comprising β-hydroxybutyrate, acetoacetate, and acetone, are metabolic products generated from fat breakdown when glucose metabolism is impaired. Studies have revealed that ketone body metabolism is intricately linked to multiple pathophysiological processes in DR, including oxidative stress, inflammatory responses, and neurodegeneration within retinal cells. This article provides a review exploring the impact of ketone body metabolism on the pathogenesis of DR, and systematically reviews the latest research progress on the impact of ketone bodies on the core pathological links such as retinal vascular barrier destruction, glial cell activation and angiogenesis through metabolic reprogramming, epigenetic modification and cell signal transduction, so as to provide a theoretical basis for in-depth understanding of the metabolic driving mechanism of DR.

西藏自治区科技计划项目(No.XZ202301YD0029C)