Table 2.

Summary of the research on the applications of iPSCs in liver disease modeling.

Strategy	Abstract	Disease Model	Conclusions	References
2D differentiation strategy	Investigated whether iPSCs from α1-antitrypsin deficiency (ATD) individuals with or without severe liver disease could model these personalized variations in hepatic disease phenotypes.	Liver disease resulting from ATD	HLCs model the individual disease phenotypes of ATD patients with more rapid degradation of misfolded ATZ and lack of globular inclusions in cells from patients who have escaped liver disease.	[49]
	A library of human iPSCs lines were generated from individuals with a range of inherited metabolic disorders (IMDs), with a focus on 3 of the diseases, and hepatocytes were derived using human iPSCs from affected patients.	IMDs of the liver	Human iPSC-derived hepatocytes successfully recapitulate key features of the cytopathology seen in related diseases, such as aggregation of misfolded mutant α1-antitrypsin in the endoplasmic reticulum, deficient LDL receptor-mediated cholesterol uptake, and elevated accumulation of cellular lipids and glycogen.	[107]
3D differentiation strategy	Generated hepatic organoids that comprise different parenchymal liver cell types and have structural features of the liver using human pluripotent stem cells.	Nonalcoholic steatohepatitis (NASH)	Developed a hepatic organoid platform with human cells that can be used to model complex liver diseases, including NASH.	[40]
	Using 11 different healthy and diseased pluripotent stem cell lines, a reproducible method was developed to obtain multicellular human liver organs composed of hepatocytes, stellate cells, and Kupffer-like cells.	Steatohepatitis	Under free fatty acid treatment, the organoid reproduced the key features of steatohepatitis, including the steatosis, inflammation, and fibrosis phenotypes.	[77]