氧化应激介导糖尿病肾病足细胞损伤机制的研究进展  

Research advance in the mechanism for oxidative stress-induced podocyte injury in diabetic kidney disease

作　　者：敖立云 谢艳云[1] AO Liyun;XIE Yanyun(Department of Nephrology,Xiangya Hospital,Central South University,Orgean Fabrosis Key Laboratory of Hunan Province,Changsha 410008,China)

机构地区：[1]中南大学湘雅医院肾病内科,湖南省器官纤维化重点实验室,长沙410008

出　　处：《中南大学学报（医学版）》2021年第12期1403-1408,共6页Journal of Central South University ：Medical Science

基　　金：国家自然科学基金(82073918,82173877);湖南省重点研发计划项目(2021SK2015);湖南省自然科学基金(2021JJ41039)。

摘　　要：糖尿病肾病(diabetic kidney disease,DKD)是糖尿病严重的微血管并发症之一,也是进展为终末期肾病的主要原因,目前临床治疗手段有限。DKD发病机制复杂,足细胞损伤是DKD的核心事件,而氧化应激与DKD足细胞损伤密切相关。在DKD中氧化应激可通过多种途径介导足细胞凋亡和裂孔隔膜损伤。抗氧化应激药物可通过减轻足细胞损伤来延缓DKD的进展。研究氧化应激介导DKD足细胞的损伤机制,可为DKD的临床治疗提供新的思路和策略。Diabetic kidney disease(DKD)is one of the serious microvascular complications of diabetes mellitus(DM),and it is also the leading cause for the end-stage kidney disease(ESKD),but the clinical treatment for it is limited at present.The pathogenesis of DKD is complex.Many studies have shown that podocyte injury is the core event of DKD,and oxidative stress is closely related to podocyte injury in DKD.Oxidative stress mediates podocyte apoptosis and slit diaphragm damage in DKD through various pathways.The antioxidant drugs can slow down the progression of DKD through reducing podocyte injury and are expected to enter clinical trials.The research status of antioxidant drugs is very important,which will provide new strategies for the clinical treatment of DKD.

关 键 词：糖尿病肾病 足细胞损伤 氧化应激 

分 类 号：R587.2[医药卫生—内分泌] R692.9[医药卫生—内科学]