Table 4 Study on bone metabolism mechanism of BMSC-exos

ADSC-exos

Rat rotator cuff injury model

It significantly improved osteogenic and adipogenic differentiation, and enhanced the expression of RUNX2, Sox-9, TNMD, TNC, and Scx as well as the mechanical properties of the articular portion

DSC-exos may promote rotator cuff repair by mediating TDSCs

[138]

BMSC-exos, BMSCs-derived exosome of miR-21-5p

miR-21-5p

Femoral bone marrow of trauma patients

BmiR-21-5p improves osteoporosis by regulating KLF3, providing a potential therapeutic strategy for osteoporosis

BMSC-exos can enhance osteoblast proliferation and improve osteoporosis through miR-21-5p-mediated KLF3 inhibition

[139]

DM-BMSC-exos

miR-140-3p

N- rat and DM- rat

Promotes the osteogenic function of BMSC, thereby accelerating the healing of diabetic wounds. MiR-140-3p promotes bone formation and accelerates bone regeneration

Normal exosomes and MIRI-140-3P overexpression -Exos promote BMSC osteogenic capability by inhibiting nerve plexus B4 expression of Sema1D receptors and the neuroprotein B1/RhoA/ROCK pathway

[140]

BMSC-exos

miR-206

OA mouse model

MSC-derived exosome miR-206 promotes the proliferation and differentiation of osteoblasts in OA by reducing Elf3

MiR-206 down-regulated and Elf3 up-regulated in OA animal and cell models

[141]

M2-Exos

Normal and diabetic rat models with bone defects

While inhibiting osteoclastogenesis in vitro, restorative M2-like macrophages can significantly protect alveolar bone from absorption in vivo

M2-Exos up-regulated the IL-10 cytokine expression in BMSC and BMDM and activated the IL-10/IL-10R pathway

[147]

CMS_Exos and static_Exos

Hind limb unloading (HU)-induced DOP mouse model

The number of tartrate TRAP positive osteoclasts was significantly reduced. CMS_Exos and static_Exos both partially saved osteoporosis caused by mechanical unloading

CMS_Exos impairs osteoclast differentiation by inhibiting RANKL-induced nuclear factor κ B (NF-κ B) signaling pathway

[148]