Phenotypic changes in non-parenchymal cells during development of liver fibrosis. (IMAGE)
Caption
In response to chronic stimuli such as alcohol abuse, viral infection, NAFLD/NASH and toxic damage, liver loses its normal structure and non-parenchymal cells including HSCs, KCs and LSECs undergo phenotypic changes. HSCs and KCs are in activation and LSECs become capillarised with loss of fenestrae and markers followed by release of fibrogenic stimuli such as TGF-β, LOX and so on, which play important roles in the development of liver fibrosis. CCL2, C-C motif chemokine ligand 2; HBV, hepatitis B virus; HCV, hepatitis C virus; HSC, hepatic stellate cell; IL, interleukin; KC, Kupffer cell; LOX, lysyl oxidase; LSEC, liver sinusoidal endothelial cell; Mito-DAMP, mitochondrial damage-associated molecular pattern; MoMF, monocyte-derived macrophage; NAFLD, non-alcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; SMA, smooth muscle actin; STING, stimulator of interferon gene; TGF, transforming growth factor; TNF, tumour necrosis factor; VCAM-1, vascular cell adhesion molecule 1.
Credit
By Yingying Liu and Lin Wang
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License
CC BY-NC