Table 1 MSC-EXOs-related miRNAs for the treatment of liver diseases
From: Advances in the treatment of liver injury based on mesenchymal stem cell-derived exosomes
Diseases | MiRNA | Model | Mechanism |
|---|---|---|---|
Liver fibrosis | miR-27b-3p | CCl4-induced mouse model | Inhibit LOXL2 as the downstream target gene of YAP [63] |
Liver fibrosis | miR-148a | CCl4-induced mouse model | Target KLF6 to control the STAT3 signaling pathway [64] |
Liver fibrosis | miR-125b | CCl4-induced mouse model | Inhibiting Smo expression and Hh signaling activation [65] |
Liver fibrosis | miR-122 | CCl4-induced mouse model | Targeting the binding site located in the 3'-UTR of P4HA1 mRNA [66] |
Liver fibrosis | miR-181-5p | CCl4-induced mouse model | Inhibit STAT3/Bcl-2/ Beclin-1 pathway [67] |
ALF | miR-455-3p | CCl4/LPS-induced mouse model | Inhibit inflammatory responses by targeting PIK3r1 [68] |
HCC | miR-199a-3p | Orthotopic HCC mouse model | Reversed the reduced phosphorylation of 4EBP1 and 70S6K in HCC cells and the reduced chemoresistance of HCC cells treated [69] |
HCC | miR-451a | human HCC cell lines Hep3B, MHCC-97 H, HB611, HepG2 and SMMC-7721 | Delay the progression of EMT by inhibiting ADAM10 [70] |
HCC | miR-15a | human HCC cell lines Hep3B and Huh7 | Downregulation of SALL4 inhibits the proliferation, migration and invasion of HCC cells [71] |
HCC | miR-122 | HepG2 cell xenograft model | Enhance the chemosensitivity of HCC [72] |
Liver oxidative stress | miR-26a-5p | cecal ligation puncture (CLP) and lipopolysaccharide (LPS) plus D-galactosamine (D-gal) as sepsis-induced ALI model | Targeting MALAT1 reduces oxidative stress [73] |
Liver oxidative stress | miR-200a | DEN-induced LF model | Preventing oxidative stress, inflammation, necroptosis and anti-fibrosis [74] |
Liver steatosis | miR-96-5p | HFD-induced mouse model | Inhibits caspase-2, thereby hindering fatty acid synthesis and lipid uptake, and upregulates fatty acid oxidation [75] |
Liver steatosis | miR-627-5p | HFHF-induced mouse model | Enhanced lipid and glucose metabolism and decreased liver damage by blocking FTO expression [76] |