Stem cell-derived exosome-mediated renal protection: halting fibrosis progression

doi:10.3877/cma.j.issn.2095-1221.2026.02.004

Abstract

Abstract:

Renal fibrosis is a multifactorial-driven pathological process involving intrarenal inflammation, cellular proliferation, and excessive deposition of collagen and fibronectin. Without intervention, this process can progress to chronic kidney disease (CKD) and may ultimately lead to end-stage renal disease. Stem cell-derived exosomes represent an emerging therapeutic strategy for renal fibrosis. Functioning as nanoscale extracellular vesicles (EVs), exosomes carry bioactive molecules that can be taken up by local or distal cells. They serve as mediators of intercellular communication while also delivering therapeutic payloads (e.g., microRNAs, proteins). In animal models of kidney disease, stem cell-derived exosomes have been demonstrated to effectively attenuate inflammation, suppress fibroblast activation, and reduce collagen production in the renal interstitium, thereby delaying fibrosis progression. This review summarizes the mechanisms underlying the antifibrotic effects of exosomes derived from various stem cell sources used as therapeutic agents for renal fibrosis. It also outlines future translational research directions and strategies aimed at enhancing the therapeutic efficacy of stem cell-derived exosomes.

Key words: Exosomes, Renal fibrosis, Cell-free therapy, Chronic kidney disease, Stem cells

Rui Fang, Shengqiang Yu. Stem cell-derived exosome-mediated renal protection: halting fibrosis progression[J]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2026, 16(02): 94-101.

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References 63

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外泌体来源	实验模型	治疗性载荷	信号通路	给药剂量、频率、方式	主要发现	参考文献
BMSCs （鼠源）	雄性Fisher344大鼠，UUO，CKD	miR-294、miR-133	TGF-β/Smad、ERK1/2	200 μg/次，术前3天1次、术后1次，静脉注射	减轻ECM沉积，抑制EMT，保护肾结构	[24]
BMSCs （人源）	雌性C57BL/6小鼠，UUO，CKD	抗miR-Let-7i-5p	TSC1/mTOR	50 μg/次，2次/周、4周，静脉注射	减轻ECM沉积，抑制EMT，改善肾功能	[25]
BMSCs （鼠源）	C57BL/6小鼠（性别未指定），UUO-CKD、IRI-AKI	miR-34c-5p	未研究	静脉注射，剂量、频率未指定	减轻成纤维细胞和巨噬细胞的活化	[28]
BMSCs （人源）	雄性SD大鼠，5/6SNx，CKD	未研究	Smurf2/Smad7	150 μg/次，1次/周、16周，静脉注射	增强si-Smurf 2作用，改善肾功能	[27]
BMSCs （人源）	雄性SD大鼠，UUO，CKD	miR-181d	NF-κB	1×10⁶ particles/次，术后1次，静脉注射	减轻肾脏纤维化	[29]
BMSCs （人源）	雄性Balb/c小鼠，UUO，CKD	未研究	未研究	30 μg/次，术后0、3、7、14、21 d各1次，静脉注射	减轻ECM沉积，减少炎症和纤维化	[26]
UC-MSCs（人源）	雄性SD大鼠，UUO，CKD	CK1δ、β-TRCP	CK1δ/β-TRCP-YAP	200 μg/只，具体未指定	减轻ECM沉积和肾纤维化	[30]
UC-MSCs（人源）	雄性SD大鼠，UUO，CKD	未研究	p38 MAPK/ERK	200 μg/次，术后1次，左肾动脉注射	减轻细胞凋亡，清除ROS	[31]
UC-MSCs（人源）	雄性C57BL/6小鼠，IRI，AKI	Oct-4	未研究	未指定	减少细胞凋亡，改善肾功能，减少纤维化	[33]
UC-MSCs（人源）	雄性C57BL/6小鼠，IRI，AKI	miR-29a-3p	未研究	50 μg/次，术前1 d和术后0、3、6、9 d各1次，静脉注射	促进血管生成，减轻肾纤维化	[34]
UC-MSCs（人源）	雄性C57BL/6小鼠，PBOO，CKD	未研究	Wnt/β-catenin	50 ~ 100 μg/次，术后7 d 1次，静脉注射	抑制了PBOO诱导的肾脏损伤和细胞增殖	[32]
ADSC （鼠源）	雄性C57BL/KsJ-db/db小鼠，DN，CKD	miR-486	Smad1/mTOR	静脉注射12周，剂量、频率未指定	促进自噬并减少足细胞凋亡，减轻DN症状	[38]
ADSC （人源）	雄性C57BL/6小鼠，CLP，AKI	未研究	SIRT1	100 μg/次，术后1次，静脉注射	减轻AKI炎症、凋亡和微循环障碍	[39]
ESCs （鼠源）	雄性C57BL/6小鼠，IRI，AKI	未研究	未研究	100 μg/次，术后1次，肾皮质注射	促进肾脏结构恢复、血管生成，保护肾功能	[40]
iPSCs （人源）	雄性C57BL/6小鼠，UUO，CKD	未研究	SIRT6/β-catenin	1×10¹¹ particles/次，术后1次，静脉注射	抑制炎症反应，改善肾功能，减轻纤维化	[41]
UDSCs （人源）	雄性SD大鼠，STZ-DN，CKD	miR-16-5p	未研究	100 μg/次，1次/周、12周，静脉注射	减轻足细胞凋亡，抑制纤维化	[42]
LSCs （人源）	雄性BALB-c小鼠，IRI，AKI	未研究	未研究	1×10 particles/次，术后0、3天各1次，静脉注射	改善炎症和肾功能，减轻EMT	[43]
hP-MSCs	雄性C57BL/6小鼠，IRI，AKI	未研究	未研究	100 μg/次，术后0、1、2、7、14 d各1次，静脉注射	修复线粒体，抑制氧化应激和肾纤维化	[44]

外泌体来源	实验模型	治疗性载荷	信号通路	给药剂量、频率、方式	主要发现	参考文献
BMSCs （鼠源）	雄性Fisher344大鼠，UUO，CKD	miR-294、miR-133	TGF-β/Smad、ERK1/2	200 μg/次，术前3天1次、术后1次，静脉注射	减轻ECM沉积，抑制EMT，保护肾结构	[24]
BMSCs （人源）	雌性C57BL/6小鼠，UUO，CKD	抗miR-Let-7i-5p	TSC1/mTOR	50 μg/次，2次/周、4周，静脉注射	减轻ECM沉积，抑制EMT，改善肾功能	[25]
BMSCs （鼠源）	C57BL/6小鼠（性别未指定），UUO-CKD、IRI-AKI	miR-34c-5p	未研究	静脉注射，剂量、频率未指定	减轻成纤维细胞和巨噬细胞的活化	[28]
BMSCs （人源）	雄性SD大鼠，5/6SNx，CKD	未研究	Smurf2/Smad7	150 μg/次，1次/周、16周，静脉注射	增强si-Smurf 2作用，改善肾功能	[27]
BMSCs （人源）	雄性SD大鼠，UUO，CKD	miR-181d	NF-κB	1×10⁶ particles/次，术后1次，静脉注射	减轻肾脏纤维化	[29]
BMSCs （人源）	雄性Balb/c小鼠，UUO，CKD	未研究	未研究	30 μg/次，术后0、3、7、14、21 d各1次，静脉注射	减轻ECM沉积，减少炎症和纤维化	[26]
UC-MSCs（人源）	雄性SD大鼠，UUO，CKD	CK1δ、β-TRCP	CK1δ/β-TRCP-YAP	200 μg/只，具体未指定	减轻ECM沉积和肾纤维化	[30]
UC-MSCs（人源）	雄性SD大鼠，UUO，CKD	未研究	p38 MAPK/ERK	200 μg/次，术后1次，左肾动脉注射	减轻细胞凋亡，清除ROS	[31]
UC-MSCs（人源）	雄性C57BL/6小鼠，IRI，AKI	Oct-4	未研究	未指定	减少细胞凋亡，改善肾功能，减少纤维化	[33]
UC-MSCs（人源）	雄性C57BL/6小鼠，IRI，AKI	miR-29a-3p	未研究	50 μg/次，术前1 d和术后0、3、6、9 d各1次，静脉注射	促进血管生成，减轻肾纤维化	[34]
UC-MSCs（人源）	雄性C57BL/6小鼠，PBOO，CKD	未研究	Wnt/β-catenin	50 ~ 100 μg/次，术后7 d 1次，静脉注射	抑制了PBOO诱导的肾脏损伤和细胞增殖	[32]
ADSC （鼠源）	雄性C57BL/KsJ-db/db小鼠，DN，CKD	miR-486	Smad1/mTOR	静脉注射12周，剂量、频率未指定	促进自噬并减少足细胞凋亡，减轻DN症状	[38]
ADSC （人源）	雄性C57BL/6小鼠，CLP，AKI	未研究	SIRT1	100 μg/次，术后1次，静脉注射	减轻AKI炎症、凋亡和微循环障碍	[39]
ESCs （鼠源）	雄性C57BL/6小鼠，IRI，AKI	未研究	未研究	100 μg/次，术后1次，肾皮质注射	促进肾脏结构恢复、血管生成，保护肾功能	[40]
iPSCs （人源）	雄性C57BL/6小鼠，UUO，CKD	未研究	SIRT6/β-catenin	1×10¹¹ particles/次，术后1次，静脉注射	抑制炎症反应，改善肾功能，减轻纤维化	[41]
UDSCs （人源）	雄性SD大鼠，STZ-DN，CKD	miR-16-5p	未研究	100 μg/次，1次/周、12周，静脉注射	减轻足细胞凋亡，抑制纤维化	[42]
LSCs （人源）	雄性BALB-c小鼠，IRI，AKI	未研究	未研究	1×10 particles/次，术后0、3天各1次，静脉注射	改善炎症和肾功能，减轻EMT	[43]
hP-MSCs	雄性C57BL/6小鼠，IRI，AKI	未研究	未研究	100 μg/次，术后0、1、2、7、14 d各1次，静脉注射	修复线粒体，抑制氧化应激和肾纤维化	[44]

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