Table 4.
Examples of EV use in preclinical studies related to the treatment of liver dysfunctions.
| Source of EVs | Model | Major outcomes | References |
|---|---|---|---|
| Human iPSCs | In vitro | Modulation of the profibrogenic transcriptome profile in activated HSCs | (193) |
| In vivo murine model of ameliorating liver disfunctions | Reduced development of fibrosis | ||
| Human UC-MSCs | In vivo murine CCl4-induced liver fibrosis model | Reduced development of fibrosis Reduced expression of collagen I and III Inactivation of TGF-b1/Smad signaling pathway |
(194) |
| Mouse hepatocytes | In vivo murine hepatic fibrogenesis model | Reduced inflammation Reduced development of fibrosis Suppressed monocyte/macrophage infiltration |
(195) |
| LX-2 | In vitro | Decreased proliferation and invasion of HCC | (196) |
| In vivo murine model of HCC | Reduced tumor size Increased apoptosis of HCC |
||
| Human AT-MSCs | In vitro | Increased chemosensitivity of HCC cells | (197) |
| In vivo murine model of HCC | Increased sensitiveness of HCC to chemotherapeutic agents |
AT-MSCs, adipose derived MSCs; HCC, hepatocellular carcinoma; HSCs, hepatic stellate cells; iPSCs, induced pluripotent stem cells; UC-MSCs, umbilical cord Wharton’s jelly MSCs.