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Table 1 Direct administration of native mesenchymal stromal cells (MSCs) in liver failure preclinical models, especially acute liver failure (ALF)

From: Mesenchymal stromal cells (MSCs) and their exosome in acute liver failure (ALF): a comprehensive review

Sources Model Result (ref)
Placenta Rat Migration to damaged site and induction of immunomodulatory effects by secreting paracrine factors in ALF [193]
Bone marrow Rat Systemic administration of MSCs reduced ALT, AST, and bilirubin levels [124]
Bone marrow Rat Reducing ALF, improving glucose metabolism and survival, and also stimulation of the hepatocyte proliferation by activating AKT/GSK-3β/β-catenin pathway [122]
Adipose tissue Rat Normalization of amino acids, sphingolipids, and glycerophospholipids in the liver and blood along with attenuation hepatocyte apoptosis and conversely promoting their proliferation rate [194]
Placenta Rat Stimulation of liver repair through the antifibrotic and autophagic mechanisms [149]
Umbilical cord Monkey Inhibition of the activity of IL-6 producing monocyte, amelioration of the liver histology, and also animal survival [119]
Adipose tissue Rat Suppression of the secondary complications of liver failure [195]
Bone marrow Porcine Improving the liver function homeostasis, attenuation of reactive oxygen species (ROS) following efficient homing, and also differentiation into hepatocytes [196]
Bone marrow Rat Amelioration of mitochondrial activities and normalization of lipid metabolism upon modifying the mTOR pathway [197]
Umbilical cord Rat Provoking the endogenous liver regeneration, hindrance of hepatocyte apoptosis by up-regulated c-Met in hepatocyte [120]
Bone marrow Rat Potentiating of MSCs-elicited liver regeneration following the abrogation of autophagy in MSCs [198]
Bone marrow Rat Amelioration of ALF by up-regulation of the heme oxygenase 1 (HO-1) expression, which resulted in inspiring the autophagy process through PI3K/AKT signaling axis [116]
Bone marrow Mice Enhancing MSCs competencies to stimulate liver recovery following transdifferentiation as well as fusion with hepatocytes by SDF-1/CXCR4 axis [199]
Bone marrow Mice Reducing ALF by IL-10 produced by MSCs, which ultimately inhibits pyroptosis [110]
Bone marrow Mice MSCs derived from adipose tissue showed superiority over MSCs isolated from bone marrow in ALF [125]
Bone marrow Mice Improvement of hepatocyte mediated by PGE2 released by MSCs, ameliorating ALF [113]
Wharton’s jelly Mice Restoration of hepatotoxicity by WJ-MSC [200]
Bone marrow Swine Averting ALF upon stimulation of hepatocyte proliferation and suppressing their apoptosis by intraportal MSCs transplantation [123]
Bone marrow Rat Attenuated aggregation and function of neutrophils [118]
Adipose tissue Mice Protection against ALF by affecting the Nrf2 and cytochrome P450 expression [201]
Umbilical cord Mice Inducing the endogenous liver regeneration but not notable hepatogenic differentiation [202]
Umbilical cord Mice Attenuation of ALF by down-regulation of MyD88/NF-κB pathway involved in inflammation [203]
Bone marrow Mice Attenuation of ALF by modifying ratio between Th17 and regulatory NKT cells [204]
  1. Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Glycogen synthase kinase-3β (GSK-3β), Mammalian target of rapamycin (mTOR), Phosphoinositide 3-kinases (PI3Ks), CXC chemokine receptor 4 (CXCR4), Stromal derived factor-1α (SDF-1α or CXCL12), Prostaglandin E2 (PGE2), Nuclear factor-erythroid factor 2-related factor 2 (Nrf2), Nuclear factor-kappa B (NF-κB), Natural killer T (NKT) cells, T helper 17 (Th17), Interleukin-10 (IL-10)