Table 1.
Cell sources
|
Passage number
|
Cell models
|
Biological effects
|
Rat BM MSCs | P3-4 | HepG2 cells | rMSCs alleviated cellular lipotoxicity and metabolic disturbance, primarily by regulating ER stress and calcium homeostasis via SERCA[34] |
Mouse BM MSCs | P5-10 | HepG2 cells | mBMSCs restored disordered glucose and lipid metabolism, as well as mitochondrial dysfunction in T2DM/NAFLD[35] |
Human UC MSCs derived miR-24-3p | Not reported | Primary hepatocytes | hUC-MSC derived miR-24-3p suppressed lipid accumulation, ROS generation, and inflammatory response through targeting KEAP-1 signaling[37] |
Human UC MSCs derived miR-627-5p | P3 | L-02 cells | hUC-MSC-derived miR-627-5p improved glucose and lipid metabolism by targeting FTO[39] |
Mouse AD MSCs derived miR-223-3p | P2 or above | NCTC1469 cells | mADSC-EV-derived miR-223-3p exhibited suppressive effects on lipid accumulation and liver fibrosis by inhibiting the target gene E2F1[42] |
Human MenSCs | P2-3 | L-02/AML12 cells | Hepatocyte growth factor secreted by MenSCs in NAFLD promoted hepatic glycogen storage and attenuated lipid accumulation through the downregulation Rnf186[43] |
Human UC MSCs derived Exos | Not reported | HepG2/AML12 cells | hUC-MSC-Exos attenuated steatosis in hepatocytes and inhibited oxidative stress in NASH[45] |
Mouse AD MSCs | P5-6 | Murine hepatocyte cell line H2.35 | mADSCs treatment alleviated lipotoxicity-induced apoptosis in steatotic hepatocytes by activating the Notch signaling pathway[46] |
Human UC MSCs derived CM | Not reported | L-02 cells | hMSC-CM enhanced liver mitochondrial function while reducing inflammation and apoptosis by upregulating SIRT1[50] |
Human UC MSCs derived Exos | P4-7 | HepRG cells | hUC-MSC-Exos reduced inflammatory cytokines by inducing macrophage anti-inflammatory phenotypes[59] |
Human CB MSCs derived Exos with curcumin | Not reported | HepG2 cells | MSC-Exos with curcumin improved cell viability and inhibited lipogenesis, while the anti-apoptotic pathway involved the downregulation of ASK1, JNK, and BAX genes[63] |
Human UC MSC derived Exos | P3-4 | L-02/AML12 cells | MSC-Exos inhibit lipid accumulation by promoting the β-oxidation of fatty acids and suppressing fatty acid synthesis[64] |
MSCs: Mesenchymal stem cells; BM: Bone marrow; UC: Umbilical cord; AD: Adipose- derived; CB: Cord blood; Exos: Exosomes; EVs: Extracellular vesicles; T2DM: Type 2 diabetes mellitus; MenSCs: Menstrual blood-derived stem cells; mADSCs: Mouse adipose-derived stem cells; NAFLD: Non-alcoholic fatty liver disease.