[1]陈 婷,刘金彦.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[J].医学信息,2022,35(22):170-175.[doi:10.3969/j.issn.1006-1959.2022.22.042]
 CHEN Ting,LIU Jin-yan.The study of PI3K/Akt/mTOR Pathway and Podocyte Autophagy in Renal Function Repair of Diabetic Nephropathy[J].Journal of Medical Information,2022,35(22):170-175.[doi:10.3969/j.issn.1006-1959.2022.22.042]
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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()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
35卷
期数:
2022年22期
页码:
170-175
栏目:
综述
出版日期:
2022-11-15

文章信息/Info

Title:
The study of PI3K/Akt/mTOR Pathway and Podocyte Autophagy in Renal Function Repair of Diabetic Nephropathy
文章编号:
1006-1959(2022)22-0170-06
作者:
陈 婷刘金彦
(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)
Author(s):
CHEN TingLIU Jin-yan
(1.School of Clinical Medicine,Jining Medical University,Jining 272067,Shandong,China;2.Department of Nephropathy,Jining No.1 People’s Hospital,Jining 272011,Shandong,China)
关键词:
糖尿病肾病足细胞自噬PI3K/Akt/mTOR通路
Keywords:
Diabetic kidney diseasePodocyteAutophagyPI3K/Akt/mTOR pathway
分类号:
R587.1
DOI:
10.3969/j.issn.1006-1959.2022.22.042
文献标志码:
A
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。
Abstract:
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.

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更新日期/Last Update: 1900-01-01