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Copyright ©The Author(s) 2024.
World J Stem Cells. Jul 26, 2024; 16(7): 760-772
Published online Jul 26, 2024. doi: 10.4252/wjsc.v16.i7.760
Table 1 Mesenchymal stem cells treatments for non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in vitro
Cell sources
Passage number
Cell models
Biological effects
Rat BM MSCsP3-4HepG2 cellsrMSCs alleviated cellular lipotoxicity and metabolic disturbance, primarily by regulating ER stress and calcium homeostasis via SERCA[34]
Mouse BM MSCsP5-10HepG2 cellsmBMSCs restored disordered glucose and lipid metabolism, as well as mitochondrial dysfunction in T2DM/NAFLD[35]
Human UC MSCs derived miR-24-3pNot reportedPrimary hepatocyteshUC-MSC derived miR-24-3p suppressed lipid accumulation, ROS generation, and inflammatory response through targeting KEAP-1 signaling[37]
Human UC MSCs derived miR-627-5pP3L-02 cellshUC-MSC-derived miR-627-5p improved glucose and lipid metabolism by targeting FTO[39]
Mouse AD MSCs derived miR-223-3pP2 or aboveNCTC1469 cellsmADSC-EV-derived miR-223-3p exhibited suppressive effects on lipid accumulation and liver fibrosis by inhibiting the target gene E2F1[42]
Human MenSCsP2-3L-02/AML12 cellsHepatocyte growth factor secreted by MenSCs in NAFLD promoted hepatic glycogen storage and attenuated lipid accumulation through the downregulation Rnf186[43]
Human UC MSCs derived ExosNot reportedHepG2/AML12 cellshUC-MSC-Exos attenuated steatosis in hepatocytes and inhibited oxidative stress in NASH[45]
Mouse AD MSCsP5-6Murine hepatocyte cell line H2.35mADSCs treatment alleviated lipotoxicity-induced apoptosis in steatotic hepatocytes by activating the Notch signaling pathway[46]
Human UC MSCs derived CMNot reportedL-02 cellshMSC-CM enhanced liver mitochondrial function while reducing inflammation and apoptosis by upregulating SIRT1[50]
Human UC MSCs derived ExosP4-7HepRG cellshUC-MSC-Exos reduced inflammatory cytokines by inducing macrophage anti-inflammatory phenotypes[59]
Human CB MSCs derived Exos with curcuminNot reportedHepG2 cellsMSC-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 ExosP3-4L-02/AML12 cellsMSC-Exos inhibit lipid accumulation by promoting the β-oxidation of fatty acids and suppressing fatty acid synthesis[64]