Cell–cell crosstalks in the liver in the development of MASLD/MASH. (IMAGE)

First Hospital of Jilin University

Cell–cell crosstalks in the liver in the development of MASLD/MASH.

Caption

Both hepatic resident cells and infiltrated immune cells are involved in the development of MASLD and MASH. It is believed that hepatocyte injuries are among the early events of MASLD pathogenesis. With the involvement of immune cells, hepatic inflammation occurs to various extents in different patients. When the inflammation is not resolved, proinflammatory factors further trigger additional reactions from other cells in the liver, including hepatic stellate cells, LSECs, cholangiocytes and immune cells. At this stage, MASLD has progressed to MASH with hallmark features of hepatic steatosis, inflammation and fibrosis. AP1, activator protein 1; BAs, bile acids; CCL2, C-C motif chemokine ligand 2; CXCL1, C-X-C motif chemokine ligand 1; DAMPs, damage-associated molecular patterns; DC, dendritic cell; DNL, de novo lipogenesis; ECM, extracellular matrix; FFA, free fatty acids; FGF1, fibroblast growth factor 1; FXR, farnesoid X receptor; ICAM1, intercellular adhesion molecule 1; IFNγ, interferon gamma; IL1/4/6/13/17/22, interleukin 1/4/6/13/17/22; LSEC, liver sinusoidal endothelial cell; MASH, metabolic dysfunction-associated steatohepatitis; MASLD, metabolic dysfunction-associated steatotic liver disease; MMP9/12, matrix metallopeptidase 9/12; MPO, myeloperoxidase; NK, natural killer; PAMPs, pathogen-associated molecular patterns; PDGFB, platelet-derived growth factor subunit B; ROS, reactive oxygen species; SMAD, SMAD family member; STAT3, signal transducer and activator of transcription 3; TAZ, transcription coactivator with PDZ-binding motif, also called WWTR1; TG, triglyceride; TGFβ, transforming growth factor beta; Th2, T helper cell 2; TNFα, tumour necrosis factor alpha; VCAM1, vascular cell adhesion molecule 1; VEGF, vascular endothelial growth factor; YAP, Yes1 associated transcriptional regulator.

Credit

By Xiaocheng Charlie Dong, et al.

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CC BY-NC

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