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

doi:10.3877/cma.j.issn.2095-3216.2023.01.007

Abstract

Abstract:

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.

Key words: MicroRNA-155, Kidney Diseases

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.

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References 42

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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]

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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