Research progress on the role of extracellular vesicles in acute kidney injury

doi:10.3877/cma.j.issn.2095-3216.2022.03.010

Abstract

Abstract:

Acute kidney injury (AKI) is a group of critical syndromes, which is caused by multiple causes and characterized by rapid decline in renal function and accumulation of metabolic waste. The incidence of AKI is increasing, and it has a high mortality rate in the intensive care unit. Currently, the clinical diagnosis of AKI is based on the level of serum creatinine and the urine output, which are not sensitive and timely to indicate renal injury. And there are no effective methods for the treatment of AKI yet. Extracellular vesicles (EVs) in the urine are derived from the renal intrinsic cells, and participate in the pathophysiological process of the kidney, playing an important role in the process of AKI. In addition, EVs are natural nano-scale membrane vesicles that can be used for targeting the kidney to deliver therapeutic molecules and alleviate the kidney damage. This article reviewed the types, recognition, and physiological functions of EVs, and focused on the diagnostic and therapeutic value of EVs in AKI.

Key words: Acute kidney injury, Extracellular vesicles, Diagnosis, Treatment

Mengting Lu, Jiaxin Bao, Changchun Cao. Research progress on the role of extracellular vesicles in acute kidney injury[J]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2022, 11(03): 167-171.

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References 43

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来源	类型	变化	诊断标志物	模型/疾病	物种
尿液	外泌体	↑	胎球蛋白A	顺铂AKI、IRI-AKI、AKI	大鼠、人
			ATF-3、ATF-3的mRNA	脓毒症AKI、顺铂AKI、IRI-AKI	小鼠、人
			有机阴离子转运蛋白5	顺铂AKI	大鼠
			钠氢交换体3	AKI	人
			miR-16、miR-24、miR-200c、miR-125、miR-351	IRI-AKI	大鼠
			miR-19b-3p	脂多糖AKI	小鼠
			miR-21	恙虫病相关AKI	人
			tRNA	IRI-AKI	小鼠
		↓	水通道蛋白-1、水通道蛋白-2	IRI-AKI	大鼠
	细胞外囊泡	↑	氨基酸、脂质	药物性AKI	大鼠
血小板	微囊泡	↑	微囊泡数量	脓毒症AKI	人
			miR-191	肾移植AKI	人、大鼠

来源	类型	变化	诊断标志物	模型/疾病	物种
尿液	外泌体	↑	胎球蛋白A	顺铂AKI、IRI-AKI、AKI	大鼠、人
			ATF-3、ATF-3的mRNA	脓毒症AKI、顺铂AKI、IRI-AKI	小鼠、人
			有机阴离子转运蛋白5	顺铂AKI	大鼠
			钠氢交换体3	AKI	人
			miR-16、miR-24、miR-200c、miR-125、miR-351	IRI-AKI	大鼠
			miR-19b-3p	脂多糖AKI	小鼠
			miR-21	恙虫病相关AKI	人
			tRNA	IRI-AKI	小鼠
		↓	水通道蛋白-1、水通道蛋白-2	IRI-AKI	大鼠
	细胞外囊泡	↑	氨基酸、脂质	药物性AKI	大鼠
血小板	微囊泡	↑	微囊泡数量	脓毒症AKI	人
			miR-191	肾移植AKI	人、大鼠

细胞来源	类型	效应分子	动物模型	作用机制
骨髓来源的间充质干细胞	细胞外囊泡	miR-200a-3p	IRI-AKI	激活Keap1-Nrf2信号通路、稳定线粒体稳态
		miR29、miR30	UUO	抑制上皮间充质转化
		miRNAs	甘油诱导AKI	促进肾小管形态恢复
	微囊泡	Bcl2、Bcl-xL、BIRC8；Casp1、Casp8、LTA	顺铂AKI	抑制肾小管上皮细胞凋亡
	外泌体	miR-125b-5p、miR-199a-3p	IRI	激活AKT、ERK信号通路、抑制细胞凋亡
脂肪来源的间充质干细胞	外泌体	沉默调节蛋白1	脓毒症AKI	减轻NF-κB介导的炎症损伤
		Sox9	IRI-AKI	促进肾小管再生
	细胞外囊泡	miR-222-3p、miR-143-5p	单侧肾狭窄	促进细胞增殖、血管生成，调节免疫
人胎盘来源的间充质干细胞	细胞外囊泡	Sox9	IRI	促进细胞再生
诱导多能干细胞	细胞外囊泡	-	IRI	改善线粒体功能、减少氧化应激
尿液来源的干细胞	外泌体	miR-146a-5p	IRI	抑制NF-κB信号传导及炎症细胞浸润
无特定来源细胞	细胞外囊泡	白介素-10	IRI	抑制肾小管上皮细胞中的mTORC1通路促进线粒体稳态；驱动巨噬细胞向M2极化
无特定来源细胞	外泌体	srIκB	IRI	减轻NF-κB介导的炎症损伤
巨噬细胞	细胞外囊泡	白介素-10	IRI	促进线粒体自噬、促进巨噬细胞极化为M2表型
红细胞	细胞外囊泡	siP65、siSnai1	IRI、UUO	减轻肾小管炎症损伤

细胞来源	类型	效应分子	动物模型	作用机制
骨髓来源的间充质干细胞	细胞外囊泡	miR-200a-3p	IRI-AKI	激活Keap1-Nrf2信号通路、稳定线粒体稳态
		miR29、miR30	UUO	抑制上皮间充质转化
		miRNAs	甘油诱导AKI	促进肾小管形态恢复
	微囊泡	Bcl2、Bcl-xL、BIRC8；Casp1、Casp8、LTA	顺铂AKI	抑制肾小管上皮细胞凋亡
	外泌体	miR-125b-5p、miR-199a-3p	IRI	激活AKT、ERK信号通路、抑制细胞凋亡
脂肪来源的间充质干细胞	外泌体	沉默调节蛋白1	脓毒症AKI	减轻NF-κB介导的炎症损伤
		Sox9	IRI-AKI	促进肾小管再生
	细胞外囊泡	miR-222-3p、miR-143-5p	单侧肾狭窄	促进细胞增殖、血管生成，调节免疫
人胎盘来源的间充质干细胞	细胞外囊泡	Sox9	IRI	促进细胞再生
诱导多能干细胞	细胞外囊泡	-	IRI	改善线粒体功能、减少氧化应激
尿液来源的干细胞	外泌体	miR-146a-5p	IRI	抑制NF-κB信号传导及炎症细胞浸润
无特定来源细胞	细胞外囊泡	白介素-10	IRI	抑制肾小管上皮细胞中的mTORC1通路促进线粒体稳态；驱动巨噬细胞向M2极化
无特定来源细胞	外泌体	srIκB	IRI	减轻NF-κB介导的炎症损伤
巨噬细胞	细胞外囊泡	白介素-10	IRI	促进线粒体自噬、促进巨噬细胞极化为M2表型
红细胞	细胞外囊泡	siP65、siSnai1	IRI、UUO	减轻肾小管炎症损伤

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