Chronic Lung Disease |
Hyperoxia-treated lung epithelial cells caused an upregulation of miR-320a and miR-221 in MVs |
[45] |
CLD causes elevated serum EV levels of miR-21 in human infants |
[46] |
Immune Response |
IL-4 causes upregulated miR-138-5p and miR-149-5p in BMDM-derived exosomes |
[48] |
Neuroinflammation |
Astrocytes stimulated with IL-1β increased exosomal levels of let-7d, miR-126, miR-130b, miR-139-5p, and miR-141-3p |
[50] |
Exosomal miR-193-3p delivered to a SAH mouse caused a reduction in HDAC3 reduced inflammation |
[52] |
Diabetes Mellitus |
Hyperglycemia causes a reduction in MV and AB-derived miR-126 and MV-derived miR-26a |
[58,59] |
Diabetic neuropathy patients demonstrate increased miR-126 within plasma-derived EVs |
[60] |
EV-mediated delivery of miR-126 improved endothelial barrier function and aids in EPC recovery |
[60,61] |
Cancer |
In A549 cells, Syndecan-1 expression caused a 184-fold upregulation of exosome-derived has-miR-485-3p, which has been shown to suppress cancer growth |
[69,70] |
Tumor-derived exosomes Dicer, which converts pre-miRNAs to mature miRNAs to promote proliferation |
[71] |
Bile-derived EVs from CCA patients have upregulated miR-191, miR-486-3p, and miR-1274b and downregulated miR-195 within the CCA cells |
[74,75] |
miR-21, miR-141, miR-200a, miR-200c, miR-200b, miR-203, miR-205, and miR-214 are upregulated in both OC tumor cells and OC-derived exosomes, while miR-205-5p, miR-145-5p, miR-10a-5p, miR-346, and miR-328-3p were all found to be upregulated exclusively in OC-derived exosomes |
[76,77] |
Heart Disease and Atherosclerosis |
Fibroblast-derived exosomes mediate cardiac hypertrophy via potential miR-21 dependent mechanism |
[81] |
miR-92a-3p, miR-222-3p, and miR-26a-5p are selectively sorted into MVs through an oxLDL-dependent mechanism |
[83] |
KLF2 assists with packaging miR-143/145 into EVs for atheroprotective effect of SMCs |
[88] |