Table 3 MSCs-EXOs as miRNAs delivery system in different diseases
MSC-EXOs | Diseases | miRNAs | Route of administration | Explain | References |
|---|---|---|---|---|---|
HUC-MSC- EXOs | Neointimal hyperplasia (NIH) | MiR-148a-3p | Intravenously injected | HUC-MSC-EXOs suppressed NIH in a mouse carotid artery ligation model, and the suppressor properties on VSMC phenotypic switching and migration interceded via transfer of miR-148a-3p to VSMCs to target Serpine1 | [142] |
UC-MSC- EXOs | Endometrial fibrosis | miR-145-5p/ZEB2 | – | This method might reverse endometrial stromal cell fibrosis by controlling miR-145-5p/ZEB2 axis, showing a possible new approach to improve endometrial regeneration | [143] |
MSC-EXOs | Renal fibrosis | anti-let-7i-5p | Intravenously injected | Anti-let-7i-5p from MSC-EXOs uses anti-fibrotic efficacy in TGF-β1-stimulated fibrogenic reactions in NRK52E cells in vitro also in the UUO-stimulated renal fibrosis model in vivo by triggering the TSC1/mTOR pathway | [144] |
BM-MSC-EXOs | Myocarditis | miR-133 | intraperitoneally injected | Increased exosomal miR-133a promoted cardiac action and prevent myocardial fibrosis, and EMT in rats with VMC also improves survival rate and suppresses apoptosis of cardiomyocytes in VMC by targeting MAML1 | [175] |
BM-MSC-EXOs | Intracerebral hemorrhage (ICH) | miR-146a-5p | Intrastriatal injection | This method could suggest neuroprotection and functional recovery afterward ICH by decreasing neuronal apoptosis and inflammation related to the suppression of microglial M1 polarization via a decrease expression of IRAK1 and NFAT5 | [145] |