Table 4.
Stem cell-derived exosomes for the treatment of diseases in plastic surgery and related specialties
| Target disease | Exosome | In vitro model & findings | In vivo model & findings | Refs. |
|---|---|---|---|---|
| Wound healing | UC-MSC-exo | PBMCs; inhibited cell proliferation, promoted Treg transformation & formation of endothelial tube | eczema mouse model; accelerated wound closure with more new epidermis & dermis and less scar; reduced integral score of skin injury and no. of lymphocyte infiltration in skin | 214 |
| adipose-MSC-exo | N/A | HDM-induced mouse model; reduced IgE, eosinophil & mast cell count, and downregulated inflammatory cytokines | 215 | |
| educated BM-MSC-exo | HUVECs; promoted angiogenesis via Akt/eNOS pathway | mice; promoted cutaneous wound healing | 216 | |
| atorvastatin-treated BM-MSC-exo | HUVECs; promoted proliferation, migration, tube formation, and VEGF level | streptozotocin-induced diabetic wound rat model; exosomal miR-221-3p facilitated wound repair by enhancing angiogenesis via Akt/eNOS pathway | 217 | |
| deferoxamine -stimulated BM-MSC-exo | HUVECs; activated the PI3K/Akt pathway via miR-126-mediated PTEN downregulation | streptozotocin-induced diabetic wound rat model; accelerated cutaneous wound healing by promoting angiogenesis | 218 | |
| EPC-exo | HMECs; enhanced proliferation, migration & tubule formation | streptozotocin-induced diabetic wound rat model; accelerated cutaneous wound healing by promoting angiogenesis via Erk1/2 pathway | 220 | |
| EPC-exo | N/A | streptozotocin-induced diabetic wound mouse model; exosomal miR-221-3p accelerated cutaneous wound healing via p53 pathway | 221 | |
| adipose-MSC-exo | HDFs; improved proliferation & migration | mice; promoted wound healing via PI3K/Akt signaling pathway | 222 | |
| adipose-MSC-exo | HaCaT cells; promoted proliferation & migration by activating Akt/HIF-1α pathway | mice; promoted wound healing, which was eliminated by inhibition of p‑Akt and HIF‑1α | 223 | |
| iPSC-exo, MSC-exo | HDFs, HaCaT cells; accelerated proliferation via ERK1/2 pathway | N/A | 224 | |
| MALAT1-adipose-MSC-exo | HaCaT cells & HDFs; promoted wound healing by miR-124 via Wnt/β-catenin pathway | N/A | 225 | |
| MSC-exo | BJ cells; promoted fibroblasts migration | rats; exosomal miR-135a promoted cutaneous wound healing by inhibiting LATS2 expression | 226 | |
| EPC-exo | HaCaT cells; promoted proliferation & migration, and inhibited apoptosis | diabetic mice; accelerated wound healing via downregulating PPARγ | 227 | |
| UC-MSC-exo | H2O2-treated HaCaT cells; increased proliferation & migration, and suppressed apoptosis | mice; attenuated full-thickness skin wounding by enhancing epidermal re-epithelialization and dermal angiogenesis via suppressing AIF nucleus translocation | 228 | |
| UC-MSC-exo | N/A | mice; suppressed myofibroblast differentiation by inhibiting TGF-β/Smad2 pathway during wound healing; miR-21, -23a, -125b, -145 responsible for preventing scar formation | 229 | |
| UC-MSC-exo | HDFs; suppressed dermal fibroblasts-myofibroblasts transition via TGF-β/Smad2/3 pathway | N/A | 230 | |
| adipose-MSC-exo | primary HDFs; stimulated proliferation, migration, and collagen synthesis | mice; exo recruited to wound area, and accelerated cutaneous wound healing; increased collagen I & III in early stage and inhibited collagen in late stage to reduce scar formation | 231 | |
| ESC-exo | HUVECs; ameliorated senescence, proliferation, and migration | D-galactose-induced aging mice; exosomal miR-200a accelerated wound closure and enhanced angiogenesis via Nrf2 activation | 232 | |
| ESC-exo | HDFs; inhibited cellular senescence via TGF-β receptor 2 pathway | mice; exosomal mmu-miR-291a-3p accelerated excisional skin wound healing process | 233 | |
| Skin flap | adipose-MSC-exo | HUVECs; increased cell proliferation, migration with more cord-like structures | I/R injury rat model; increased flap survival & capillary density, and decreased inflammatory reaction & apoptosis; H2O2-conditioned exo were better | 234 |
| Craniofacial defect | SCAP-exo | HUVECs; improved angiogenic capacity and cell migration | mice; promoted craniofacial soft tissue regeneration by enhancing Cdc42-mediated vascularization | 235 |
| Scleroderma | UC-MSC-exo | N/A | mice; attenuated myofibroblast activation and collagen deposition in dermal fibrosis by downregulating the TGF-β/Smad signaling pathway | 236 |
| Leishmaniasis | UC-MSC-exo + Aloe-Emodin | L929 & J744 cells, artificial wound model; healed 72% wound in 24 h | L.major promastigotes & amastigotes; inhibited for 4–10 folds; combinations superior to exo alone | 237 |
| Alopecia | NSC-exo | dermal papilla cells; exosomal miR-100 promoted cell proliferation | depilation-induced mice hair regeneration model; promoted hair follicle growth by activating Wnt/β-catenin pathway | 238 |
AIF apoptosis-inducing factor, Akt protein kinase B, BM bone marrow, eNOS endothelial nitric oxide synthase, EPC endothelial progenitor cell, ESC embryonic stem cell, exo exosome, HDF human dermal fibroblasts, HDM house dust mite, HIF hypoxia-inducible factor, HMEC human microvascular endothelial cell, HUVEC human umbilical vein endothelial cell, I/R ischemia-reperfusion, LATS large tumor suppressor, MALAT metastasis associated lung adenocarcinoma transcript, miR microRNA, MSC mesenchymal stem cell, NSC neural stem cell, PBMC peripheral blood mononuclear cell, PI3K phosphoinositide 3-kinase, PTEN phosphatase & tensin homolog, SCAP stem cells from apical papilla, TGF transforming growth factor, Treg regulatory T cell, UC umbilical cord, VEGF vascular endothelial growth factor