晚期糖基化终产物促进慢性肾脏病进展的作用及防治策略  

Advanced glycation end products in chronic kidney disease:pathogenic role and preventive strategy

作　　者：杨莹 蔡广研[1] Yang Ying;Cai Guang-Yan(Department of Nephrology,the First Medical Center of Chinese PLA General Hospital/Chinese PLA Institute of Nephrology/State Key Laboratory of Kidney Diseases,National Center for Clinical Medical Research on Chronic Nephropathy,Beijing 100853,China)

机构地区：[1]解放军总医院第一医学中心肾脏病科、解放军肾脏病研究所、肾脏疾病国家重点实验室、国家慢性肾病临床医学研究中心,北京100853

出　　处：《解放军医学杂志》2020年第5期554-558,共5页Medical Journal of Chinese People's Liberation Army

基　　金：国家重点研发计划课题(2018YFA0108803);国家973计划课题(2015CB553605);北京市科技计划课题(D181100000118004)。

摘　　要：晚期糖基化终产物(AGE)是一类由还原糖与蛋白质之间的自发非酶促反应产生的稳定化合物,近年来被证实与多种慢性疾病相关。在慢性肾脏病(CKD)中,AGE可通过改变蛋白质的生理功能、触发细胞级联反应,导致滤过屏障解体、引发氧化应激和肾脏纤维化,加重CKD的进展。反过来,CKD的进展导致肾功能下降,随后由于肾小球滤过率的下降而使AGE进一步累积,形成恶性循环。AGE在CKD发生发展过程中的作用是近年来研究的热点。该文旨在阐述AGE的生化特性、相关细胞事件、在CKD发展中的作用及相关防治策略的研究进展。Advanced glycation end products (AGE) are stable compounds produced by spontaneous non-enzymatic reaction between reducing sugars and proteins,and have been proven recent years to be associated with a variety of chronic diseases.AGE can exacerbate the progression of chronic kidney disease (CKD) by altering the physiological function of proteins,triggering cellular cascade reaction,leading to the disintegration of the filtration barrier,causing oxidative stress and renal fibrosis.The progression of CKD,in turn,leads to a decline in renal function,followed by further accumulation of AGE due to a decrease in glomerular filtration rate,forming a vicious circle.The role of AGE in the occurrence and development of CKD is a hot topic in recent years.Here’s a description of AGE biochemical characteristics,related cellular events,role in CKD development,and current research progress on AGE therapy.

关 键 词：晚期糖基化终产物 慢性肾脏病 糖尿病肾病 

分 类 号：R5587.1[医药卫生—血液循环系统疾病]