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Table 1 Summary of the mitochondrial dysfunction modulation of MSCs in liver disease

From: A new perspective on mesenchymal stem cell-based therapy for liver diseases: restoring mitochondrial function

Liver disease

Mitochondrial dysfunction

Source

Delivery route

Potential mechanism

Ref

NAFLD

Abnormal lipid metabolism and calcium homeostasis

Human bone marrow

Intrasplenic injection

Mitochondrial transfer via TNT

[8]

Rat bone marrow

Tail vein

Restoring sarcoplasmic/ER Ca2+ ATPase activity to alleviate of ER stress

[46]

CCl4-induced liver injury

Oxidant/antioxidant imbalance

Human bone marrow

Tail vein

Increasing SOD activity and inhibiting ROS production

[47]

Human umbilical cord

Tail vein

Presented more distinct antioxidant by EVs

[48]

APAP and H2O2-induced liver injury

Oxidant/antioxidant imbalance

Rat bone marrow

Intrahepatic injection

Fractionated MSC exosomes reduce ROS activity more efficiently

[49]

Oxidant/antioxidant imbalance

Mouse adipose tissue

Tail vein

Increasing hepatic GSH level and alleviate ROS accumulation

[10]

D-galactose induced liver injury

Oxidant/antioxidant imbalance

Human umbilical cord

Tail vein

Reducing oxidative stress via activation of Nrf2/HO-1 pathway

[50]

Hepatic I/R injury

Oxidant/antioxidant imbalance

Human umbilical cord

Tail vein

Suppressing oxidative stress by MnSOD encapsulated in EVs

[21]

Impaired mitophagy

Human umbilical cord

Peripheral vein

Reducing Parkin and PINK1 expression and inactivating AMPKα pathway

[22]

Post-hepatectomy liver failure

Impaired mitochondrial dynamics

Mouse bone marrow

Portal vein

Downregulating p-Drp1 and FIS1 expression and upregulating MFN2

[7]

Abnormal lipid metabolism

Reducing mitochondrial damage and secreting IL-10

Liver cirrhosis

Abnormal lipid metabolism

Human placenta

Tail vein

Attenuating ER stress via activating the EGFR-PI3K-CaM Pathway by PRL-1

[51]