Table 3.
Summary of angiogenesis-related studies involving adipose-derived mesenchymal stem/stromal cell-derived extracellular vesicles.
| Context | Source of ASC | Authors | Effect of ASC EVs |
|---|---|---|---|
| Angiogenesis | Human | [127] | Stimulate in vitro and in vivo angiogenesis. PDGF enhances EV secretion in ASCs. |
| Angiogenesis | Human | [129] | Promote angiogenesis in vitro and in vivo via miRNA-31. |
| Angiogenesis | Human | [12] | Promote angiogenesis in vitro and in vivo via miRNA-125a. |
| Angiogenesis, fat grafting | Human | [128] | Promote angiogenesis and fat grafting in vivo. |
| Angiogenesis, fat grafting | Human | [130] | Improve survival of fat graft by angiogenesis promotion via let-7/argonaute 1/VEGF pathway. |
| Angiogenesis, fat grafting | Mouse | [131] | ASC-EVs comparable to ASCs in aiding fat graft survival via angiogenesis promotion and fat graft volume retention. |
| Wound healing | Human | [13] | Promote in vivo wound healing via activation of the AKT and ERK pathways. Promote angiogenesis. |
| Wound healing, diabetic environment | Human | [132] | Healthy EVs can upregulate the expression of genes important to wound healing. Enhance the mobility of diabetic ASCs to the wound site in vitro and in vivo. |
| Wound healing, diabetic environment | Human | [133] | Promote wound healing in a diabetic foot ulcer model in vivo. Enhanced effect with nuclear factor-E2-related factor 2 (Nrf2) |
| Wound healing, diabetic environment | Mouse | [134] | Exosome containing wound-healing gel promotes wound healing and angiogenesis in diabetic environment in vivo. |
| Wound healing, diabetic environment | Human | [135] | mmu_circ_0000250-modified ASC-EVs promote wound healing in vivo. |
| Myocardial infarction | Rat | [23] | miRNA-126 overexpression prevents myocardial damage and promotes angiogenesis in vivo. |
| Myocardial infarction | Mouse | [136] | SIRT-overexpressing ASC-EVs promote survival and myocardial function by promoting angiogenesis via Nrf2 in vivo. |
| Myocardial infarction | Human | [137] | Inhibit cardiomyocyte apoptosis, reduce infarction area and increase microvascular density in vivo. |
| Obesity | Human | [138] | Obesity decreases pro-angiogenic effect of EVs via impairment of miR-126 content. |
| Hypoxia, angiogenesis | Rat | [139] | Promote angiogenesis via miRNA-181b in oxygen–glucose deprivation in vitro. |
| Hypoxia, angiogenesis | Human | [140] | Hypoxia treatment of ASCs promotes EV-induced angiogenesis via protein kinase A (PKA) signaling pathway. |
| Hypoxia, angiogenesis, fat grafting | Human | [141] | Promote survival of fat graft by promoting angiogenesis and reducing inflammation. Hypoxia pretreatment of ASCs can enhance the effects. |
| Hypoxia, angiogenesis, fat grafting | Human | [142] | Hypoxia treatment of ASCs promotes EV-induced angiogenesis and fat grafting in vivo. |
| Hypoxia, angiogenesis | Human | [143] | EVs from hypoxia-conditioned ASCs are a more potent angiogenesis inducer than EVs without preconditioning. |