糖尿病肾病足细胞损伤机制的研究进展  

Research Progress in Mechanism of Podocyte Injury in Diabetic Nephropathy

作　　者：王娜[1] 邹大威[2] WANG Na;ZOU Dawei(Capital Medical University,Beijing 100069,China;School of Traditional Chinese Medicine,Capital Medical University,Beijing 100069,China)

机构地区：[1]首都医科大学,北京100069 [2]首都医科大学中医药学院,北京100069

出　　处：《医学综述》2019年第20期4087-4092,共6页Medical Recapitulate

基　　金：北京市自然科学基金(7172032)

摘　　要：糖尿病肾病是糖尿病的慢性微血管并发症之一,其主要临床表现为蛋白尿和肾功能进行性衰退,最终会发展为肾衰竭。足细胞作为肾小球滤过屏障的最后一层,其结构和功能的完整性与蛋白尿关系密切。近年来,关于足细胞损伤与糖尿病肾病关系的研究取得了较大进展。氧化应激可直接导致足细胞凋亡,或改变微血管通透性最终导致足细胞损伤。此外,足细胞微RNA及自噬水平的异常也会导致足细胞损伤,外泌体也可通过细胞内化作用影响足细胞的结构及功能。Diabetic nephropathy is one of the chronic microvascular complications of diabetes mellitus. The main clinical manifestations are proteinuria and progressive deterioration of renal function,which will eventually develop into renal failure. As the last layer of glomerular filtration barrier,podocytes are closely related to proteinuria in terms of structural and functional integrity. In recent years,great progress has been made in the study of the relationship between podocyte injury and diabetic nephropathy. Oxidative stress can directly lead to podocyte apoptosis,or alter microvascular permeability leading to podocyte injury. In addition,abnormal levels of podocyte microRNAs and autophagy can cause podocyte damage,and exosomes can also affect the structure and function of podocytes through cell internalization.

关 键 词：糖尿病肾病 足细胞损伤 氧化应激 微RNA 自噬 

分 类 号：R692.6[医药卫生—泌尿科学]