Table 4 Summary of studies on the role of extracellular vesicles in skin injury.
EVs source | Target cells or tissues | Animal model | Molecular mechanism | Action effect | Ref |
|---|---|---|---|---|---|
hADSC-Exos | – | Full-thickness skin defect model | Down-regulate TNF-α, IL-6, CD14, CD19, CD68, and C-caspase 3, up-regulate VEGF, CD31, Ki67, PCNA, filaggrin, loricrin and AQP3 | Accelerate skin wound healing | [114] |
hBMSC-Exos | HaCaT cells and HSFs | Full-thickness skin wounds injury model in rats | Target on TGF-β/Smad signaling pathway, but increased the expression of TGF-β3 and Smad7 | Improve scar formation and promote wound healing | [115] |
FDMSC-Exos | ADFs | Full-thickness dermal wound injury model | Inhibit MMP-13, ADAMTS5 and iNOS | Reinduce the expression of type II collagen, aggrecan, and protected mice from joint damage | [116] |
hBMSC-Exos and JMMSC-Exos | Macrophages | Skin Wound-Healing | By carrying miR-223 targeting Pknox1 | Induced macrophages toward M2 polarization and promote wound healing | [117] |
mag-BMSC-Exos | HUVECs and HSFs | Rat Skin Wound Model | Highly-express miR-21-5p and target SPRY2 to activating PI3K/AKT and ERK1/2 signaling pathways | Accelerate skin wound healing | [118] |
hUCMSCs-EVs | HaCaT cells and HSFs | Cutaneous wound mouse model | Highly-express miR-27b p and promote the expression of JUNB and IRE1α by targeting the Itchy E3 ubiquitin-protein ligase (ITCH) | Accelerate cutaneous wound healing | [119] |
hUCMSC-Exos | Myofibroblast | Full-thickness skin defect mouse model | Highly-express microRNAs (miR-21, -23A, -125b and -145) repressed the TGF-β2 /SMAD2 pathway | Attenuate excess myofibroblast formation and anti-scarring | [120] |
hADSC-Exos | HaCaT cells and HSFs | Wound healing of skin-injured mice | Highly-express miR-19b regulated TGF-β pathway by targeting CCL1 | Promote the healing of skin wounds | [121] |
hADSC-Exos | HSFs | Full-thickness skin defects in the backs of rats | Down-regulate the expression of Col1, Col3, α-SMA, IL-17RA, and P-SMad2 / P-SMad3, and up-regulate the level of SIP1, while overexpression miR-192-5p target inhibition of IL-17RA expression | Reduce the level of pro-fibrosis protein, improve hypertrophic scar fibrosis and accelerate wound healing | [122] |
hADSC-EVs | HSFs and HMECs | – | Overexpression miR-486-5p inhibit Sp5 and elevate the CCND2 expression | Promote proliferation, migration and reduce apoptosis | [123] |
hAMSC-Exos | Fibroblasts | Full-thickness skin defects in the backs of rats | Downregulation of LATS2 after overexpression of miR-135a | Increase cell migration and promote wound healing | [124] |
