线粒体自噬与NLRP3炎症小体的相互作用在糖尿病视网膜病变中作用的研究进展  

Progress in role of interaction between mitophagy and NLRP3 inflammasome in diabetic retinopathy injury

作　　者：王亦山[1] 罗向霞[1] 苏莉[1] 柳青 WANG Yishan;LUO Xiangxia;SU Li;LIU Qing(Ophthalmology Department of Gansu Provincial Hospital of TCM,Gansu 730000,China)

机构地区：[1]甘肃省中医院眼科,甘肃兰州730000

出　　处：《中国病理生理杂志》2025年第3期600-605,共6页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.82360955)。

摘　　要：糖尿病视网膜病变(DR)是糖尿病患者常见的严重微血管并发症之一,其主要病理特征包括视网膜血管损伤、氧化应激和慢性炎症反应。近年来,越来越多的研究表明,线粒体自噬在维持视网膜细胞的功能稳态和防止氧化损伤中发挥着重要作用,而核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)是DR中促炎性反应的关键调节因子。线粒体自噬通过清除受损线粒体,减少线粒体源性活性氧(ROS)的过度产生,进而抑制NLRP3炎症小体的激活。相反,线粒体功能障碍会导致NLRP3炎症小体的过度激活,进一步加剧视网膜的炎症反应和细胞凋亡。因此,本文综述了线粒体自噬与NLRP3炎症小体在DR中的独立作用及其相互调控机制,为以线粒体自噬和NLRP3炎症小体为靶点的研究提供参考资料。Diabetic retinopathy(DR)is one of the common serious microvascular complications in diabetic patients,with the main pathological features of retinal vascular injury,oxidative stress and chronic inflammatory response.In recent years,more and more studies have shown that mitophagy plays an important role in maintaining the functional homeostasis of retinal cells and preventing oxidative damage,and nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)is a key regulator of pro-inflammatory response in DR.Mitophagy can reduce the excessive production of reactive oxygen species(ROS)by removing damaged mitochondria,thereby inhibiting the activation of NLRP3 inflammasome.In contrast,mitochondrial dysfunction can lead to excessive activation of NLRP3 inflammasome,which further aggravates the inflammatory response and apoptosis of the retina.Therefore,this article reviews the independent role of mitophagy and NLRP3 inflammasome in DR and their mutual regulatory mechanisms,so as to provide reference for the study of mitophagy and NLRP3 inflammasome as targets.

关 键 词：糖尿病视网膜病变 线粒体自噬 NLRP3炎症小体 

分 类 号：R587.2[医药卫生—内分泌] R774.1[医药卫生—内科学] R363[医药卫生—临床医学]