{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,14]],"date-time":"2025-05-14T01:41:51Z","timestamp":1747186911136,"version":"3.40.5"},"reference-count":29,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2023,7,4]],"date-time":"2023-07-04T00:00:00Z","timestamp":1688428800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100012964","name":"Minist\u00e8re de l\u2019Enseignement Sup\u00e9rieur et de la Recherche Scientifique","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100012964","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005413","name":"Universit\u00e9 Paris Descartes","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005413","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2023,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background &amp; Aims<\/jats:title><jats:p>Patients with non\u2010alcoholic fatty liver disease (NAFLD) have impaired liver regeneration. Liver endothelial cells play a key role in liver regeneration. In non\u2010alcoholic steatohepatitis (NASH), liver endothelial cells display a defect in autophagy, contributing to NASH progression. We aimed to determine the role of endothelial autophagy in liver regeneration following liver resection in NAFLD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>First, we assessed autophagy in primary endothelial cells from wild type mice fed a high fat diet and subjected to partial hepatectomy. Then, we assessed liver regeneration after partial hepatectomy in mice deficient (<jats:italic>Atg5<\/jats:italic><jats:sup><jats:italic>lox\/lox<\/jats:italic><\/jats:sup>;<jats:italic>VE\u2010cadherin\u2010Cre<\/jats:italic><jats:sup><jats:italic>+<\/jats:italic><\/jats:sup>) or not (<jats:italic>Atg5<\/jats:italic><jats:sup><jats:italic>lox\/lox<\/jats:italic><\/jats:sup>) in endothelial autophagy and fed a high fat diet. The role of endothelial autophagy in liver regeneration was also assessed in <jats:italic>ApoE<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> hypercholesterolemic mice and in mice with NASH induced by methionine\u2010 and choline\u2010deficient diet.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>First, autophagy (LC3II\/protein) was strongly increased in liver endothelial cells following hepatectomy. Then, we observed at 40 and 48\u2009h and at 7\u2009days after partial hepatectomy, that <jats:italic>Atg5<\/jats:italic><jats:sup><jats:italic>lox\/lox<\/jats:italic><\/jats:sup>;<jats:italic>VE\u2010cadherin\u2010Cre<\/jats:italic><jats:sup><jats:italic>+<\/jats:italic><\/jats:sup> mice fed a high fat diet had similar liver weight, plasma AST, ALT and albumin concentration, and liver protein expression of proliferation (PCNA), cell\u2010cycle (Cyclin D1, BrdU incorporation, phospho\u2010Histone H3) and apoptosis markers (cleaved Caspase\u20103) as <jats:italic>Atg5<\/jats:italic><jats:sup><jats:italic>lox\/lox<\/jats:italic><\/jats:sup> mice fed a high fat diet. Same results were obtained in <jats:italic>ApoE<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> and methionine\u2010 and choline\u2010deficient diet fed mice, 40\u2009h after hepatectomy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These results demonstrate that the defect in endothelial autophagy occurring in NASH does not account for the impaired liver regeneration occurring in this setting.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.15665","type":"journal-article","created":{"date-parts":[[2023,7,5]],"date-time":"2023-07-05T03:16:12Z","timestamp":1688526972000},"page":"2309-2319","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Endothelial autophagy is not required for liver regeneration after partial hepatectomy in mice with fatty liver"],"prefix":"10.1111","volume":"43","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6928-7431","authenticated-orcid":false,"given":"Adel","family":"Hammoutene","sequence":"first","affiliation":[{"name":"Universit\u00e9 Paris Cit\u00e9, PARCC, INSERM  Paris France"},{"name":"Universit\u00e9 Paris\u2010Cit\u00e9, Inserm, Centre de recherche sur l'inflammation, UMR 1149  Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marion","family":"Tanguy","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Cit\u00e9, PARCC, INSERM  Paris France"},{"name":"Universit\u00e9 Paris\u2010Cit\u00e9, Inserm, Centre de recherche sur l'inflammation, UMR 1149  Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M\u00e9lanie","family":"Calmels","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Cit\u00e9, PARCC, INSERM  Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Riccardo","family":"Pravisani","sequence":"additional","affiliation":[{"name":"Service de chirurgie h\u00e9patobiliaire et pancr\u00e9atique H\u00f4pital Beaujon, AP\u2010HP  Clichy France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miguel","family":"Albuquerque","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris\u2010Cit\u00e9, Inserm, Centre de recherche sur l'inflammation, UMR 1149  Paris France"},{"name":"Service d'Anatomie Pathologique H\u00f4pital Beaujon, Assistance Publique\u2010H\u00f4pitaux de Paris  Clichy France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christophe","family":"Casteleyn","sequence":"additional","affiliation":[{"name":"Department of Morphology, Imaging, Orthopaedics, Physiotherapy and Nutrition Ghent University  Ghent 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