PI3K/Akt/mTOR通路与足细胞自噬在糖尿病肾病肾功能修复中的研究  

The study of PI3K/Akt/mTOR Pathway and Podocyte Autophagy in Renal Function Repair of Diabetic Nephropathy

作　　者：陈婷 刘金彦[2] CHEN Ting;LIU Jin-yan(School of Clinical Medicine,Jining Medical University,Jining 272067,Shandong,China;Department of Nephropathy,Jining No.1 People's Hospital,Jining 272011,Shandong,China)

机构地区：[1]济宁医学院临床医学院,山东济宁272067 [2]济宁市第一人民医院肾内科,山东济宁272011

出　　处：《医学信息》2022年第22期170-175,共6页Journal of Medical Information

摘　　要：糖尿病肾病(DKD)是机体长期糖、脂代谢紊乱引起的肾脏损伤。足细胞损伤是导致蛋白质漏出,肾脏纤维化的直接原因。自噬是足细胞的自我保护机制,可识别并清除受损、衰老的细胞器与生物大分子物质,调节细胞增殖与代谢。在DKD个体中,自噬相关蛋白表达减少,肾小球足细胞的稳态难以维持。现有研究表明,PI3K/Akt/mTOR信号通路通过自噬途径促进细胞自我修复。本文旨在对多种因子共同参与PI3K/Akt/mTOR通路调节自噬,延缓肾功能恶化做出归纳总结,以期为药物研发以及肾功能修复治疗提供参考。Diabetic kidney disease(DKD)is a kidney injury caused by long-term glucose and lipid metabolism disorders.Podocyte injury is the direct cause of protein leakage and renal fibrosis.Autophagy is a self-protective mechanism of podocytes that recognizes and clears damaged and aging organelles and biological macromolecules and regulates cell proliferation and metabolism.In DKD individuals,the expression of autophagy-related proteins decreased,glomerular podocyte homeostasis is difficult to maintain.Studies have shown that the PI3K/Akt/mTOR signaling pathway promotes cell self-repair through autophagy.This article aims to summarize the multiple factors involved in the PI3K/Akt/mTOR pathway to regulate autophagy and delay the deterioration of renal function,and provide reference for drug development and renal function repair treatment.

关 键 词：糖尿病肾病 足细胞 自噬 PI3K/Akt/mTOR通路 

分 类 号：R587.1[医药卫生—内分泌]