Overview of in vitro modelling strategies for major hepatic pathologies. (IMAGE)
Caption
This schematic outlines the key mechanisms, modelling approaches, platforms and phenotypic readouts commonly used for in vitro models of steatosis (MASLD), drug-induced hepatotoxicity (DILI), fibrogenesis, tumourigenesis, cholestatic injury and viral hepatic injury. Created with biorender.com. 2D, two dimensional; 3D, three dimensional; ALDH1, aldehyde dehydrogenase 1; ALT, alanine aminotransferase; APAP, acetaminophen; α-SMA, alpha-smooth muscle actin; AST, aspartate aminotransferase; BSEP, bile salt export pump; cccDNA, covalently closed circular DNA; CD44, CD44 molecule (Indian blood group); COL1A1, collagen type I alpha 1 chain; CPT1, carnitine palmitoyltransferase 1A; CYP450, cytochrome P450; DILI, drug-induced liver injury; ECM, extracellular matrix; EMT, epithelial–mesenchymal transition; ER, endoplasmic reticulum; FFA, free fatty acids; GCDCA, glycochenodeoxycholic acid; GSH, glutathione; hpi, hours post infection; HSC, hepatic stellate cell; IC50, half maximal inhibitory concentration; LCA, lithocholic acid; MASLD, metabolic dysfunction-associated steatotic liver disease; pgRNA, pregenomic RNA; ROS, reactive oxygen species; TAZ, transcriptional co-activator with PDZ-binding motif; TEER, transepithelial electrical resistance; TG, triglyceride; TGF, transforming growth factor; TMRE, tetramethylrhodamine ethyl ester; TNF, tumour necrosis factor; UPR, unfolded protein response; YAP, yes-associated protein.
Credit
By Qi Rao, Lei Wang, Frank Tacke, Adrien Guillot, Nan Ma
Usage Restrictions
Credit must be given to the creator. Only noncommercial uses of the work are permitted.
License
CC BY-NC