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] |