{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(7)"],"submitter":["Gil-Pitarch C"],"pubmed_abstract":["Drug-induced liver injury (DILI) is a significant cause of acute liver failure (ALF) and liver transplantation in the Western world. Acetaminophen (APAP) overdose is a main contributor of DILI, leading to hepatocyte cell death through necrosis. Here, we identified that neddylation, an essential post-translational modification involved in the mitochondria function, was upregulated in liver biopsies from patients with APAP-induced liver injury (AILI) and in mice treated with an APAP overdose. MLN4924, an inhibitor of the neuronal precursor cell-expressed developmentally downregulated protein 8 (NEDD8)-activating enzyme (NAE-1), ameliorated necrosis and boosted liver regeneration in AILI. To understand how neddylation interferes in AILI, whole-body biotinylated NEDD8 (<sup>bio</sup>NEDD8) and"],"journal":["Cell reports. Medicine"],"pagination":["101653"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11293357"],"repository":["biostudies-literature"],"pubmed_title":["Neddylation inhibition prevents acetaminophen-induced liver damage by enhancing the anabolic cardiolipin pathway."],"pmcid":["PMC11293357"],"pubmed_authors":["Rodriguez-Agudo R","Martinez-Cruz LA","Mercado-Gomez M","Reeves HL","Simon J","Sutherland JD","Pena-Sanfelix P","Lachiondo-Ortega S","Porcelli M","Aspichueta P","Martinez-Chantar ML","Mosca L","Rejano-Gordillo CM","Masson S","Iruzubieta P","Delgado TC","Zapata-Pavas LE","Azkargorta M","Lucena MI","Conter C","Nogueiras R","Serrano-Macia M","Andrade RJ","Gonzalez-Recio I","Crespo J","Gil-Pitarch C","Xirodimas D","Aurrekoetxea I","Goikoetxea-Usandizaga N","McCain MV","Barrio R","Mayor U","Elortza F"],"additional_accession":[]},"is_claimable":false,"name":"Neddylation inhibition prevents acetaminophen-induced liver damage by enhancing the anabolic cardiolipin pathway.","description":"Drug-induced liver injury (DILI) is a significant cause of acute liver failure (ALF) and liver transplantation in the Western world. Acetaminophen (APAP) overdose is a main contributor of DILI, leading to hepatocyte cell death through necrosis. Here, we identified that neddylation, an essential post-translational modification involved in the mitochondria function, was upregulated in liver biopsies from patients with APAP-induced liver injury (AILI) and in mice treated with an APAP overdose. MLN4924, an inhibitor of the neuronal precursor cell-expressed developmentally downregulated protein 8 (NEDD8)-activating enzyme (NAE-1), ameliorated necrosis and boosted liver regeneration in AILI. To understand how neddylation interferes in AILI, whole-body biotinylated NEDD8 (<sup>bio</sup>NEDD8) and","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-03T00:56:41.252Z","creation":"2025-04-19T20:46:48.41Z"},"accession":"S-EPMC11293357","cross_references":{"pubmed":["39019009"],"doi":["10.1016/j.xcrm.2024.101653"]}}