MSC-EXOs | Type of diseases | miRNAs | Route of administration | Explain | References |
---|---|---|---|---|---|
BM-MSC-EXOs | Diabetic peripheral neuropathy (DPN) | miR-146a (EXO-146a) | Intravenously injected via a tail vein | BM-MSCs-EXOs as biologic carriers of miR-146a can efficiently intercede and improve the curative action of MSCs in diabetic mice | [136] |
HAD-MSC-EXOs | Diabetic wound | miR-21-5p | Injected intraperitoneally (i.p.) | This method improves the production and migration of keratinocytes by the Wnt/β-catenin pathway in vitro and speeds up diabetic wound recovery via enhancing re-epithelialization, collagen repair, angiogenesis, and vessel maturation in vivo | [172] |
BM-MSC-EXOs | Autoimmune hepatitis | miR-223-3p | Injected intraperitoneally (i.p.) | BM-MSC-EXOs was effectively loaded with miR-223-3p and transported miR-223-3p into macrophages. Furthermore, there was the absence of side effects of EXOs on the macrophages | [135] |
BM-MSC-EXOs | Alzheimer’s disease | miR-146a | Intracerebroventricular injection | Researchers showed that BM-MSCs ameliorate cognitive disorder in an Alzheimer’s disease model by enhancing the expression of microRNA-146a in a part of the limbic lobe | [139] |
HUC-MSC-EXOs | Alzheimer’s disease | miR-223 | – | HUC-MSC-EXOs miR-223 preserved neuronal cells from apoptosis via the PTEN-PI3K/Akt pathway and offered a powerful curative method for Alzheimer’s disease | [173] |
AD-MSC-EXOs | Parkinson's disease | miR-188-3p | Injected intraperitoneally (i.p.) | AD-MSCs-EXOs to deliver miR-188-3p for therapy inhibited autophagy and pyroptosis while enhancing proliferation by binding to CDK5 and NLRP3 in mice and MN9D cells | [140] |
synovial MSC-EXOs | Degenerative arthritis | miR-140-5p | Intra-articular injection | This method increased the proliferation and migration of articular chondrocytes without harming extracellular matrix release in vitro. In contrast, in vivo, SMSC-EXOs miR-140-5p effectively inhibited osteoarthritis in an animal model | [174] |