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. 2021 May 26;321(1):G67–G74. doi: 10.1152/ajpgi.00009.2021

Figure 1.

Figure 1.

Liver sinusoidal endothelial cell (LSEC), a key player in hepatic inflammation in nonalcoholic steatohepatis (NASH). Lipotoxic stress, proinflammatory cytokines and chemokines, and the gut microbiome promote LSEC release of proinflammatory cytokines and chemokines and enhance the expression of adhesion molecules. Lipotoxic hepatocyte-derived extracellular vesicles (EVs) are enriched with CXCL10, ITGα9β1, and Vanin-1 and promote monocyte-derived macrophage chemotaxis and adhesion to LSECs. These EVs also elicit a proangiogenic signaling. Vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM-1), and the monoamine oxidase vascular adhesion protein-1 (VAP-1) on the LSEC surface mediate leukocyte adhesion and homing in the NASH liver. The vascular endothelial growth factor (VEGF) and angiopoietin/Tie2 pathways are activated in NASH and enhance angiogenesis.