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. 2022 Jun 28;13:936196. doi: 10.3389/fimmu.2022.936196

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Copyright © 2022 Du and Wang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Sinusoidal crosstalk mediated by LSECs play a key role in progression of NASH to liver fibrosis. A series of pathophysiological processes from NASH to liver fibrosis are mediated by LSECs. Capillarization and dysfunction of LSECs appear in early stage of NASH. Capillarized LSECs acquire a pro-inflammatory phenotype, recruiting immune cells including neutrophils, monocytes and lymphocytes to the hepatic microenvironment, promoting HCs steatosis and cell death, activating HSCs and KCs, and promoting liver fibrosis.