糖尿病性角膜病变(DK)并不是一种严重的临床疾病或病理改变,然而许多患者却因并发DK而致视力降低或丧失。因此作为一种潜在的致盲性疾病,探讨其发病机制以及探索对其有效的防治措施是很重要的。近年来,国外对DK的研究给予了一定的关注,但其发病机制尚未完全阐明。经实验和临床研究证实,醛糖还原酶(AR)作为多元醇通路的关键限速酶,与其发病密切相关。其机制可能是,AR活性增高使多元醇通路代谢增强,由此启动高渗应激、葡萄糖及脂质氧化应激、蛋白质的非酶糖基化单独或损伤协同作用。就AR与DK关系的研究进展作一综述。 Diabetic keratopathy (DK) is not a serious clinical disease or pathological change, however, many patients experience decreased or loss of vision due to concurrent DK. Therefore, as a potential blinding disease, it is very important to explore its pathogenesis and to explore its effective prevention and treatment measures. In recent years, foreign research on DK has given some attention, but its pathogenesis has not been fully elucidated. Experimental and clinical studies have confirmed that aldose reductase (AR) as the key rate-limiting enzyme in the polyol pathway is closely related to its pathogenesis. The mechanism may be that increased AR activity enhances polyol pathway metabolism, thereby initiating hypertonic stress, glucose and lipid oxidative stress, and protein nonenzymatic glycosylation alone or in concert with injury. The research progress on the relationship between AR and DK is reviewed.