Table 5.
Anti-inflammatory miRNAs in EPC-EVs
| Anti-inflammatory factor | EPC phenotype | Mechanism of action | Refs. |
|---|---|---|---|
| miR -126 | CD34+/CD133+ | ↓IL-6, IFNγ, TNF-α, L-10, VCAM1 and MCP-1 | 92 |
| miR-218-5p and miR-363-3p | CD34+/CD133+ |
↓ chemokine CCL26 by targeting p120‐catenin subfamilies ↓ IL-6, ICAM-1, and IL-1β by suppression of the NOX4-dependent p38 MAPK pathway and targeting JMY-related apoptosis |
103 |
| miR-221-3p | CD34+/CD133+ |
↑VEGF, CD31, and Ki67 ↓ AGE-induced cell hypertrophy, apoptosis, the inflammatory response |
107 |
| miR-222-3p | CD34+/CD133+ | ↑ M2 polarization | 98 |
| miR-30d-5p | Cultured EPCs | ↑ M2 polarization | 108 |
| miR-486-5p | ECFCs |
↓inflammatory cell recruitment ↑Akt phosphorylation |
111 |
| miR-21-5p | Cultured EPCs | ↓RUNX1 and TLR-4, resulting in anti-inflammatory feedback | 112 |
| TUG1 | Cultured EPCs |
↑SIRT1 ↑ M2polarization ↓Inflammatory cytokines |
97 |
| miR-126-3p and 5p | ECFCs |
↑ SPRED1, PI3K/Akt/GSK3β and RAF/ERK1/2 axis ↓ HMGB1, VCAM1, and VEGFα |
109,110,117 |