Table 1.
Disease
|
Treatment
|
Source
|
Animal
|
Main results
|
Mechanism
|
Ref.
|
ALF | APAP | Human UC-MSCs | Mice | Alleviate hepatic injury and improve survival rates | Mediate paracrine effects, regulate inflammatory response | Liu et al[38], 2014 |
ALF | LPS | Human UC-MSCs | Monkeys | Improve the hepatic histology, systemic homeostasis, and survival | Suppress the hepatic aggregation and maturation of circulating monocytes and their IL-6 secretion | Guo et al[40], 2019 |
LC | CCl4 | Human UC-MSCs | Rats | Improve liver transaminases and synthetic function, reduce liver histopathology, and reverse hepatobiliary fibrosis | Differentiate into hepatocytes | Zhang et al[3], 2017 |
LC | CCl4 | Monkey BM-MSCs | Mice | Decrease liver fibrosis, progression, and hepatocyte necrosis | Mediate paracrine effects | Fu et al[42], 2018 |
LC | TAA | Human BM-MSCs | Rats | Decrease collagen proportionate area and the content of hepatic hydroxyproline | Mediate TGF-β1/Smad signaling pathway | Jang et al[41], 2014 |
NAFLD | HFD | Mice BM-MSCs | Mice | Decrease fibrosis markers and pro-inflammatory cytokines | Regulate inflammatory process | Ezquer et al[46], 2011 |
NAFLD | HFD | Mice BM-MSCs | Mice | Decrease weight gain, expansion of subcutaneous adipose tissue, steatosis, lobular inflammation, and liver fibrosis | Suppress the proliferation of CD 4+ T cells | Wang et al[47], 2018 |
MSCs: Mesenchymal stem cells; AFL: Acute liver failure; LC: Liver cirrhosis; NAFLD: Non-alcoholic fatty liver disease; APAP: Acetaminophen; LPS: α-amatoxin and lipopolysaccharide; TAA: Thioacetamide; HFD: High-fat diet; BM-MSCs: Bone marrow-derived MSCs; UC-MSCs: Umbilical cord-derived MSCs.