Table 3.

Examples of EV use in preclinical studies related to the treatment of kidney diseases.

Source of EVs	Model	Major outcomes	References
K-MSCs	In vivo AKI murine model	Promoted angiogenesis Decreased cell apoptosis	(173)
Murine BM-MSCs	In vitro	Reversed changes in the morphology and expression of E-cadherin and α-SMA in HK2 cells	(174)
	In vivo murine CKD model	Protection against unilateral ureteral obstruction Enhancement of the expression of α-SMA and E-cadherin in kidney Reduced tubular damage
	In vitro	Suppressed ER stress Protection of cells against damage and apoptosis Promoted proliferation of renal tubular epithelium	(175)
	In vivo murine kidney I/R model	Suppressed ER stress Protection against renal I/R injury
	In vitro	Attenuated morphological changes and restored EMT in HK2 cells	(176)
	In vivo murine UUO model	Ameliorated renal function Decreased interstitial lymphocyte infiltration
Murine AT-MSCs	In vivo murine AKI model	Promoted functional kidney recovery Decreased apoptosis of tubular epithelial cells	(177)
	In vivo rat CKD model	Reduced pathological changes and renal fibrosis Protection of kidneys against inflammation, mitochondrial dysfunction, and apoptosis	(178)
Rat BM-MSCs	In vitro	Prevented SMAD2/3 and ERK1/2 phosphorylation in HK2 cells	(179)
	In vivo rat CKD model	Inhibition of renal fibrosis Ameliorated renal function and morphology

AKI, acute kidney injury; AT-MSCs, adipose derived MSCs; BM-MSCs, bone marrow MSCs; CKD, chronic kidney disease; EMT, epithelial-mesenchymal transition; ER, endoplasmic reticulum; HK2, human kidney 2 cells; I/R, ischaemia-reperfusion; K-MSCs, kidney-derived MSCs; UUO, unilateral ureteral obstruction; αSMA, alpha smooth muscle actin.