Table 1 Molecular mechanism of MSCs-derived EVs in the treatment of OP.
Source of EVs | Terminology | Cargo and modifications | Model | Effect | Ref. |
|---|---|---|---|---|---|
BMMSCs | Exosomes | Natural | Radiation-induced rat models | Promote the expression of β-catenin in BMMSCs | [67] |
Exosomes | Natural | OVX mice | Improve OP by promoting the proliferation of osteoblasts | [68] | |
Exosomes | MiR-186 | OVX rats | Promote osteogenesis | [69] | |
Apoptotic bodies | Not revealed | OVX mice | Ameliorate the reduced bone mass phenotype | [71] | |
Apoptotic bodies | MiR-1324 | OVX mice | Stimulate bone regeneration in defect areas | [72] | |
Microvesicles | MiR-31 | In vitro | Inhibit the osteogenic differentiation of MSCs | [73] | |
ADSCs | EVs | MiR-21-5p | OVX mice | Inhibit osteoclast differentiation and reduce gene expression associated with bone resorption | [92] |
Exosomes | No application | In vitro | Antagonize H/SD induced osteocyte apoptosis and osteocyte-mediated osteoclastogenesis | [93] | |
Exosomes | No application | Diabetic OP models | Suppress NLRP3 inflammasome activation in osteoclasts, and reduce bone resorption | [94] | |
Exosomes | Not revealed | GIOP rats | Alleviate apoptosis and oxidative stress and prevent the development of GIOP | [95] | |
UCMSCs | EVs | Not revealed | HLU-induced DOP rat models | Prevent bone loss and maintaining bone strength | [101] |
Exosomes | Not revealed | OVX mice | Promote BMMSC proliferation and osteogenesis through the AKT signaling pathway | [102] |
