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A moderate dose of APAP is effective for fever and pain relief; however, an overdose induces acute liver injury. The mechanism underlying APAP\u2010induced acute liver failure is unclear, and its treatment is limited. A recent report has shown that several oxidized phospholipids are associated with APAP\u2010induced acute liver failure. Lysophosphatidylcholine acyltransferase 3 (\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    ,\n                    <jats:italic>Lplat12<\/jats:italic>\n                    ), which is highly expressed in the liver, preferentially catalyzes the incorporation of arachidonate into lysophospholipids (PLs). In the present study, we investigated the roles of\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    on APAP\u2010induced acute liver injury using liver\u2010specific\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    \u2010knockout mice. Hepatic\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    deficiency reduced the degree of APAP\u2010induced necrosis of hepatocytes around Zone 3 and ameliorated the elevation of hepatic injury serum marker levels, and prolonged survival. Lipidomic analysis showed that the accumulation of oxidized and hydroperoxidized phospholipids was suppressed in\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    \u2010knockout mice. The amelioration of APAP\u2010induced acute liver injury was due not only to the reduction in the lipid synthesis of arachidonic acid PLs because of\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    deficiency, but also to the promotion of the APAP detoxification pathway by facilitating the conjugation of glutathione and N\u2010acetyl\u2010p\u2010benzoquinone imine. Our findings suggest that\n                    <jats:italic>Lpcat3<\/jats:italic>\n                    is a potential therapeutic target for treating APAP\u2010induced acute liver injury.\n                  <\/jats:p>","DOI":"10.1096\/fj.202301744r","type":"journal-article","created":{"date-parts":[[2023,11,29]],"date-time":"2023-11-29T10:24:20Z","timestamp":1701253460000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["<scp>LPCAT3<\/scp>\n                    \/\n                    <scp>LPLAT12<\/scp>\n                    deficiency in the liver ameliorates acetaminophen\u2010induced acute liver injury"],"prefix":"10.1096","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6309-9023","authenticated-orcid":false,"given":"Natsuko F.","family":"Inagaki","sequence":"first","affiliation":[{"name":"Department of Chemical System Engineering, Graduate School of Engineering The University of Tokyo  Tokyo Japan"},{"name":"Department of Lipid Signaling National Center for Global Health and Medicine  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroki","family":"Nakanishi","sequence":"additional","affiliation":[{"name":"Lipidome Lab Co., Ltd.  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