{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T22:38:15Z","timestamp":1789771095520,"version":"4.0.1"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2019,12,30]],"date-time":"2019-12-30T00:00:00Z","timestamp":1577664000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Monoacylglycerol lipase (MGL) is the last enzymatic step in triglyceride degradation, hydrolyzing monoglycerides into glycerol and fatty acids (FAs) and converting 2\u2010arachidonoylglycerol into arachidonic acid, thus providing ligands for nuclear receptors as key regulators of hepatic bile acid (BA)\/lipid metabolism and inflammation. We aimed to explore the role of MGL in the development of cholestatic liver and bile duct injury in mouse models of sclerosing cholangitis, a disease so far lacking effective pharmacological therapy.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>To this aim we analyzed the effects of 3,5\u2010diethoxycarbonyl\u20101,4\u2010dihydrocollidine (DDC) feeding to induce sclerosing cholangitis in wild\u2010type (WT) and knockout (MGL<jats:sup>\u2212\/\u2212<\/jats:sup>) mice and tested pharmacological inhibition with JZL184 in the multidrug resistance protein 2 knockout (<jats:italic toggle=\"yes\">Mdr2\u2212\/\u2212\n                                 <\/jats:italic>) mouse model of sclerosing cholangitis. Cholestatic liver injury and fibrosis were assessed by serum biochemistry, liver histology, gene expression, and western blot characterization of BA and FA synthesis\/transport. Moreover, intestinal FAs and fecal microbiome were analyzed. Transfection and silencing were performed in Caco2 cells. MGL<jats:sup>\u2212\/\u2212<\/jats:sup> mice were protected from DDC\u2010induced biliary fibrosis and inflammation with reduced serum liver enzymes and increased FA\/BA metabolism and \u03b2\u2010oxidation. Notably, pharmacological (JZL184) inhibition of MGL ameliorated cholestatic injury in DDC\u2010fed WT mice and protected <jats:italic toggle=\"yes\">Mdr2\u2212\/\u2212\n                                 <\/jats:italic> mice from spontaneous liver injury, with improved liver enzymes, inflammation, and biliary fibrosis. <jats:italic toggle=\"yes\">In vitro<\/jats:italic> experiments confirmed that silencing of MGL decreases prostaglandin E<jats:sub>2<\/jats:sub> accumulation in the intestine and up\u2010regulates peroxisome proliferator\u2013activated receptors alpha and gamma activity, thus reducing inflammation.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Collectively, our study unravels MGL as a metabolic target, demonstrating that MGL inhibition may be considered as potential therapy for sclerosing cholangitis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.30929","type":"journal-article","created":{"date-parts":[[2019,9,10]],"date-time":"2019-09-10T19:43:00Z","timestamp":1568144580000},"page":"1750-1765","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":23,"title":["Monoacylglycerol Lipase Inhibition Protects From Liver Injury in Mouse Models of Sclerosing Cholangitis"],"prefix":"10.1097","volume":"71","author":[{"given":"Matteo","family":"Tardelli","sequence":"first","affiliation":[{"name":"Hans Popper Laboratory of Molecular Hepatology,Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5006-5473","authenticated-orcid":false,"given":"Francesca V.","family":"Bruschi","sequence":"additional","affiliation":[{"name":"Hans Popper Laboratory of Molecular Hepatology,Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia D.","family":"Fuchs","sequence":"additional","affiliation":[{"name":"Hans Popper Laboratory of Molecular Hepatology,Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thierry","family":"Claudel","sequence":"additional","affiliation":[{"name":"Hans Popper Laboratory of Molecular Hepatology,Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Auer","sequence":"additional","affiliation":[{"name":"Hans Popper Laboratory of Molecular Hepatology,Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria","family":"Kunczer","sequence":"additional","affiliation":[{"name":"Hans Popper Laboratory of Molecular Hepatology,Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maximilian","family":"Baumgartner","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology,Department of Internal Medicine III,Medical University of Vienna,Vienna,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Onne","family":"A.H.O. 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