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. 2015 Sep 10;6(9):e1879. doi: 10.1038/cddis.2015.248

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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ER stress activates NLRP3 inflammasome and hepatocyte death in liver disorders. Endotoxinemia (LPS), a pathological condition found in chronic liver diseases, overwhelms hepatic IRE1α and PERK activities, leading to the overexpression of CHOP, which regulates the expression of caspase-1, caspase-11 and Puma, and triggers hepatocyte pyroptosis and apoptosis. TUDCA increased the [GRP78/CHOP] ratio, promoting protection against ER-dependent NLRP3 inflammasome and cell death pathways. Using TUDCA, either alone or combined with hepatoprotective and anti-inflammatory interventions, could be a valid therapeutic strategy for the treatment of liver disorders