Table 5 Efficacy and molecular mechanisms of EVs derived from MSCs used to treat OA in vivo and in vitro

Human S-MSCs

S-MSC-140-EVs treatment is superior to treatment with SMSC-EVs

SMSC-140-EVs promote chondrocyte proliferation and migration via RalA but do not disrupt ECM secretion

[73]

Human MSCs

MSC-EVs promote cartilage repair better than EVs after lncRNA-KLF3-AS1 knockout

EVs enriched with the lncRNA KLF3-AS1 promote cell proliferation and inhibit apoptosis

[156]

Rat MSCs

TGF-β1-treated EVs promote cartilage repair to a greater extent, and miR-135b inhibitors inhibit the treatment effects

TGF-β1 promotes chondrocyte proliferation through miR-135b enriched in MSC-EVs by regulating Sp1 expression

[81]

Human ESC-MSCs

Protect cartilage and bone from degeneration

Exert similar chondroprotective and anti-inflammatory effects

[21]

Mouse bone marrow MSCs

Prevent cartilage destruction and the process of OA

Maintain the chondrocyte phenotype by increasing COL2A1 synthesis and decreasing ADAMTS-5 expression

[83]

hBM-MSCs

MSC-92a-EVs inhibit the progression of early OA and prevent articular cartilage damage better than MSC-EVs

MSC-92a-EVs increase chondrocyte proliferation and matrix gene expression and target Wnt5A expression

[151]

Human IPFP-MSCs

Protect articular cartilage from damage and improve gait abnormalities; mir-100-5p in the EVs targets the mTOR pathway

Inhibit cell apoptosis and increase matrix synthesis partially by inhibiting mTOR to improve the level of autophagy

[78]

Human MSCs

Not mentioned

Increase the expression of COL2A1 and aggrecan expression and decrease the expression of MMP-13 and Runx2 in OA chondrocytes, attenuate apoptosis in OA articular chondrocytes and lncRNA-KLF3-AS1 targeting of the miR-206/GIT1 axis in EVs

[19]

Rat BM-MSCs

The repair effects on the EV group were significantly better than those on the BMSC and model groups

EVs transfected with siRNA-Piezo1 promote the differentiation of BM-MSCs into cartilage

[157]