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中华肾病研究电子杂志 ›› 2023, Vol. 12 ›› Issue (01) : 39 -43. doi: 10.3877/cma.j.issn.2095-3216.2023.01.007

综述

微小RNA-155在肾脏疾病中的作用研究进展
李德伦1, 袁思宇2, 刘安琪3,()   
  1. 1. 115000 营口养和医院
    2. 301617 天津中医药大学中药学院
    3. 550002 贵阳,贵州省人民医院干医科
  • 收稿日期:2022-03-09 出版日期:2023-02-28
  • 通信作者: 刘安琪

Progress of research on the role of microRNA-155 in renal diseases

Delun Li1, Siyu Yuan2, Anqi Liu3,()   

  1. 1. Yingkou Yanghe Hospital, Yingkou 115000, Liaoning Province
    2. Tianjin University of Traditional Chinese Medicine, Tianjin 301617
    3. Guizhou People′s Hospital, Guiyang 550002, Guizhou Province; China
  • Received:2022-03-09 Published:2023-02-28
  • Corresponding author: Anqi Liu
引用本文:

李德伦, 袁思宇, 刘安琪. 微小RNA-155在肾脏疾病中的作用研究进展[J]. 中华肾病研究电子杂志, 2023, 12(01): 39-43.

Delun Li, Siyu Yuan, Anqi Liu. Progress of research on the role of microRNA-155 in renal diseases[J]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2023, 12(01): 39-43.

微小RNA-155(miR-155)是一个典型的多功能基因,可参与多种生理和病理过程。越来越多的研究表明,miR-155与肾脏疾病的进展和恢复均密切相关。本文综述近年来miR-155与多种肾脏疾病关系的相关研究,包括急性肾损伤、狼疮性肾炎、IgA肾病、糖尿病肾病、慢性肾功能不全、终末期肾病等,以探讨利用miR-155作为肾脏疾病治疗潜在靶点的可能性。

MicroRNA-155 (miR-155) is a typical multifunctional gene, which can participate in a variety of physiological and pathological processes. More and more studies have shown that miR-155 is closely related to the progress and recovery of kidney diseases. This article reviewed the relevant studies on the relationship between miR-155 and various kidney diseases in recent years, including acute kidney injury, lupus nephritis, IgA nephropathy, diabetes nephropathy, chronic renal insufficiency, end-stage renal disease, etc, so as to explore the possibility of using miR-155 as a potential target for the treatment of kidney diseases.

表1 微小RNA-155在肾脏疾病中的变化及其作用机制
疾病 研究对象 微环境 表达 靶标 信号通路 作用机制 参考文献
AKI IR-AKI大鼠肾脏组织中/缺氧复氧(H/R)NRK-52E细胞中 缺氧 上调 TCF4 TCF4/Wnt/β-catenin 促进增殖;促进凋亡 [6]
AKI IR小鼠肾脏巨噬细胞分泌的外泌体中 缺氧 上调 SOCS1 NF-κB 促进炎症 [7]
AKI UUO小鼠肾脏中/TGF-β1处理的HK2细胞中 上调 iNOS-NO/TGF-β1 iNOS-NO/miR-155/TGF-β1/smad 促进EMT [8]
AKI UUO小鼠肾脏中/TGF-β1处理的HK2细胞中 上调 PDE3A PDE3A/TGF-β1/Smad 促进EMT [9]
AKI LPS处理的小鼠肾脏/LPS处理的HK2细胞中 炎性 上调 PUMA NF-κB/miR-155/Bcl-2 促进凋亡 [10]
IgA肾病 IgAN患者肾脏及尿液中 上调 [19]
IgA肾病 IgAN患者外周血单个核细胞中 下调 [21]
IgA肾病 IgAN患者尿沉渣中 下调 [20]
DN 高糖处理HRGEC细胞中 高糖 上调 ETS-1 ETS-1/VCAM-1/MCP-1/cleaved caspase-3 促进炎症;促进凋亡 [5]
DN DN患者尿液中 高糖 上调 [22]
DN DN患者尿液外泌体中 高糖 上调 [24]
DN DN患者肾脏组织中/高糖处理HRGEC细胞中 高糖 上调 TNF-α/TGF-β1-NF-κB 促进炎症 [27]
DN DN患者血清中 高糖 下调 [25]
DN DN小鼠肾脏中 高糖 上调 SOCS1 SOCS1/IL-17/nephrin 促进氧化应激 [28]
DN 高糖刺激HK2细胞中 高糖 上调 SIRT1 p53/miR155/SIRT1 抑制自噬 [30]
CKD 慢性间歇性缺氧小鼠肾脏/慢性间歇性缺氧HK2细胞中 缺氧 上调 FOXO3a FOXO3a/NLRP3 促进氧化应激;促进凋亡;促进炎症 [33]
CKD CKD男性患者血清中 上调 [35]
CKD CKD-MBD小鼠的血管平滑肌细胞中 下调 SOCS1/MITF/PU.1 [34]
ESRD 肾移植大鼠血浆中 上调 [37]
肾移植 肾移植排斥患者的尿液中 上调 [40]
肾移植 间质纤维化和肾小管萎缩患者血浆中 上调 [41]
肾移植 T细胞介导的排斥反应患者肾脏组织中 上调 [42]
RCC RCC患者/RCC细胞的外囊泡中 缺氧 上调 FOXO3 抑制FOXO3的表达 促进增殖 [4]
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