{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ouyang SX"],"funding":["Fundamental Research Funds for the Central Universities","Shanghai Shuguang Program","Shanghai \"Rising Stars of Medical Talent\" Youth Development Program-Youth Medical Talents-Clinical Pharmacist Program","National Natural Science Foundation of China","Shanghai Science and Technology Commission","Shanghai Municipal Three Year Action Plan for Strengthening the Construction of Public Health System"],"pagination":["e2305715"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11040357"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(16)"],"pubmed_abstract":["Drug-induced liver injury (DILI) is a significant global health issue that poses high mortality and morbidity risks. One commonly observed cause of DILI is acetaminophen (APAP) overdose. GSDME is an effector protein that induces non-canonical pyroptosis. In this study, the activation of GSDME, but not GSDMD, in the liver tissue of mice and patients with APAP-DILI is reported. Knockout of GSDME, rather than GSDMD, in mice protected them from APAP-DILI. Mice with hepatocyte-specific rescue of GSDME reproduced APAP-induced liver injury. Furthermore, alterations in the immune cell pools observed in APAP-induced DILI, such as the replacement of TIM4<sup>+</sup> resident Kupffer cells (KCs) by monocyte-derived KCs, Ly6C<sup>+</sup> monocyte infiltration, MerTk<sup>+</sup> macrophages depletion, "],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Gasdermin-E-Dependent Non-Canonical Pyroptosis Promotes Drug-Induced Liver Failure by Promoting CPS1 deISGylation and Degradation."],"pmcid":["PMC11040357"],"funding_grant_id":["19140904900","82104530","81971306","82073915","SHWRS(2020)_087","GWVI-11.2-XD06","22120210560","82274030","91849135","21S11901200","2019CXJQ03","19SG32","19140904700","21XD1424900"],"pubmed_authors":["Liu J","Ouyang SX","Fu JT","Sun SJ","Wu JW","Liu Y","Wang P","Zhu JH","Zhang Z","Zhang Y","Chen YT","Li DJ","Shen FM","Tong J","Zhang JB","Cao Q"],"additional_accession":[]},"is_claimable":false,"name":"Gasdermin-E-Dependent Non-Canonical Pyroptosis Promotes Drug-Induced Liver Failure by Promoting CPS1 deISGylation and Degradation.","description":"Drug-induced liver injury (DILI) is a significant global health issue that poses high mortality and morbidity risks. One commonly observed cause of DILI is acetaminophen (APAP) overdose. GSDME is an effector protein that induces non-canonical pyroptosis. In this study, the activation of GSDME, but not GSDMD, in the liver tissue of mice and patients with APAP-DILI is reported. Knockout of GSDME, rather than GSDMD, in mice protected them from APAP-DILI. Mice with hepatocyte-specific rescue of GSDME reproduced APAP-induced liver injury. Furthermore, alterations in the immune cell pools observed in APAP-induced DILI, such as the replacement of TIM4<sup>+</sup> resident Kupffer cells (KCs) by monocyte-derived KCs, Ly6C<sup>+</sup> monocyte infiltration, MerTk<sup>+</sup> macrophages depletion, ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-06-01T23:56:10.833Z","creation":"2026-05-24T03:07:32.069Z"},"accession":"S-EPMC11040357","cross_references":{"pubmed":["38417117"],"doi":["10.1002/advs.202305715"]}}