{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T17:34:34Z","timestamp":1767893674368,"version":"3.49.0"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2020,10,22]],"date-time":"2020-10-22T00:00:00Z","timestamp":1603324800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2020,10,22]],"date-time":"2020-10-22T00:00:00Z","timestamp":1603324800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Liver Transpl."],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>Nonalcoholic fatty liver disease (NAFLD) is becoming the most common indication for liver transplantation. The growing prevalence of NAFLD not only increases the demand for liver transplantation, but it also limits the supply of available organs because steatosis predisposes grafts to ischemia\/reperfusion injury (IRI) and many steatotic grafts are discarded. We have shown that monoacylglycerol acyltransferase (MGAT) 1, an enzyme that converts monoacylglycerol to diacylglycerol, is highly induced in animal models and patients with NAFLD and is an important mediator in NAFLD\u2010related insulin resistance. Herein, we sought to determine whether <jats:italic toggle=\"yes\">Mogat1<\/jats:italic> (the gene encoding MGAT1) knockdown in mice with hepatic steatosis would reduce liver injury and improve liver regeneration following experimental IRI. Antisense oligonucleotides (ASO) were used to knockdown the expression of <jats:italic toggle=\"yes\">M<\/jats:italic>\n                           <jats:italic toggle=\"yes\">o<\/jats:italic>\n                           <jats:italic toggle=\"yes\">gat1<\/jats:italic> in a mouse model of NAFLD. Mice then underwent surgery to induce IRI. We found that <jats:italic toggle=\"yes\">M<\/jats:italic>\n                           <jats:italic toggle=\"yes\">ogat1<\/jats:italic> knockdown reduced hepatic triacylglycerol accumulation, but it unexpectedly exacerbated liver injury and mortality following experimental ischemia\/reperfusion surgery in mice on a high\u2010fat diet. The increased liver injury was associated with robust effects on the hepatic transcriptome following IRI including enhanced expression of proinflammatory cytokines and chemokines and suppression of enzymes involved in intermediary metabolism. These transcriptional changes were accompanied by increased signs of oxidative stress and an impaired regenerative response. We have shown that <jats:italic toggle=\"yes\">M<\/jats:italic>\n                           <jats:italic toggle=\"yes\">ogat1<\/jats:italic> knockdown in a mouse model of NAFLD exacerbates IRI and inflammation and prolongs injury resolution, suggesting that <jats:italic toggle=\"yes\">Mogat1<\/jats:italic> may be necessary for liver regeneration following IRI and that targeting this metabolic enzyme will not be an effective treatment to reduce steatosis\u2010associated graft dysfunction or failure.<\/jats:p>","DOI":"10.1002\/lt.25886","type":"journal-article","created":{"date-parts":[[2020,9,21]],"date-time":"2020-09-21T07:15:16Z","timestamp":1600672516000},"page":"116-133","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":20,"title":["Monoacylglycerol Acyltransferase 1 Knockdown Exacerbates Hepatic Ischemia\/Reperfusion Injury in Mice With Hepatic Steatosis"],"prefix":"10.1097","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6915-1163","authenticated-orcid":false,"given":"Kim H. H.","family":"Liss","sequence":"first","affiliation":[{"name":"Departments of Pediatrics,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shelby E.","family":"Ek","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics,Washington University School of Medicine,St. Louis,MO"},{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew J.","family":"Lutkewitte","sequence":"additional","affiliation":[{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Terri A.","family":"Pietka","sequence":"additional","affiliation":[{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mai","family":"He","sequence":"additional","affiliation":[{"name":"Pathology and Immunology,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Priya","family":"Skaria","sequence":"additional","affiliation":[{"name":"Pathology and Immunology,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric","family":"Tycksen","sequence":"additional","affiliation":[{"name":"Genome Technology Access Center,McDonnell Genome Institute,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel","family":"Ferguson","sequence":"additional","affiliation":[{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Valerie","family":"Blanc","sequence":"additional","affiliation":[{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark J.","family":"Graham","sequence":"additional","affiliation":[{"name":"Ionis Pharmaceuticals, Inc.,Carlsbad,CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Angela M.","family":"Hall","sequence":"additional","affiliation":[{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0401-0463","authenticated-orcid":false,"given":"Mitchell R.","family":"McGill","sequence":"additional","affiliation":[{"name":"Department of Environmental and Occupational Health,Fay W. Boozman College of Public Health,University of Arkansas for Medical Sciences,Little Rock,AR"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kyle S.","family":"McCommis","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology,Saint Louis University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5411-3674","authenticated-orcid":false,"given":"Brian N.","family":"Finck","sequence":"additional","affiliation":[{"name":"Medicine,Washington University School of Medicine,St. Louis,MO"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","published-online":{"date-parts":[[2020,10,22]]},"reference":[{"key":"lt25886-bib-0001-20241017","doi-asserted-by":"crossref","first-page":"73","DOI":"10.1002\/hep.28431","article-title":"Global epidemiology of nonalcoholic fatty liver disease\u2010Meta\u2010analytic assessment of prevalence, incidence, and 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