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Table 2 Anti-fibrotic effect of EVs in different models

From: Extracellular vesicles: emerging roles, biomarkers and therapeutic strategies in fibrotic diseases

Origin

Cargos in EVs

Model

Mechanism

Function

Ref.

BMMSCs

undefined

mouse cGVHD

↓Th17 cells, ↑Treg

prolong the survival, diminish the clinical

and pathological scores, ameliorate fibrosis in the skin, lung, and liver

[120]

BMMSCs

miR-34c-5p

mouse UUO

↓core fucosylation

reduce renal interstitial fibrosis

[124]

BMMSCs

MFG-E8

rat UUO

↓RhoA/ROCK pathway

reduce pathological changes and renal fibrosis

[126]

hucMSCs, BMMSCs

undefined

mouse BPD

modulate the pulmonary macrophage phenotype from “M1-like” to “M2-like”

restore lung architecture, decrease pulmonary fibrosis

[121, 122]

hucMSCs

CK1δ/β-TRCP

rat UUO

↑YAP degradation

lessen collagen deposition, alleviate renal fibrosis.

[125]

PL-MSCs

miR-29c

mouse DMD

↓myoblast differentiation, ↓TGF-β

decrease fibrosis in the diaphragm and cardiac muscles

[123]

CDCs

undefined

rat Aging

undefined

attenuate left ventricular hypertrophy and fibrosis, improve diastolic function

[128]

CDCs

miR-146a-5p

Pig DCM

undefined

promote cardiomyocyte proliferation, enhance angiogenesis, reduced myocardial fibrosis. reduce myocardial fibrosis

[129]

CDCs

miR-4488

mouse ACM

↓NF-κB

improve cardiac function, reduce cardiac inflammation and fibrosis, suppress arrhythmogenesis

[130]

CDCs

undefined

pig MI

undefined

decrease scarring, halt adverse remodelling and improve left ventricular ejection fraction

[131]

CDCs

undefined

pig VA

undefined

decrease myocardial scar, suppress slowly conducting electrical pathways, inhibit VA

[132]

CDCs

undefined

rat MI

undefined

transform fibroblast phenotype from inert cells to therapeutically active cells, reduce scar mass

[133]