{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T20:22:28Z","timestamp":1793823748359,"version":"4.6.1"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2023,2,17]],"date-time":"2023-02-17T00:00:00Z","timestamp":1676592000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/ http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims:<\/jats:title>\n            <jats:p>Mixed lineage kinase domain\u2010like pseudokinase (MLKL), a key terminal effector of necroptosis, also plays a role in intracellular vesicle trafficking that is critical for regulating liver inflammation and injury in alcohol\u2010associated liver disease (ALD). Although <jats:italic toggle=\"yes\">receptor interacting protein kinase 3 (Rip3)<\/jats:italic>\n                                 <jats:sup>\n                                    \u2212\/\u2212\n                                 <\/jats:sup> mice are completely protected from ethanol\u2010induced liver injury, <jats:italic toggle=\"yes\">Mlkl<\/jats:italic>\n                                 <jats:sup>\n                                    \u2212\/\u2212\n                                 <\/jats:sup> mice are only partially protected. Therefore, we hypothesized that cell\u2010specific functions of MLKL may contribute to ethanol\u2010induced injury.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results:<\/jats:title>\n            <jats:p>Bone marrow transplants between <jats:italic toggle=\"yes\">Mlkl<\/jats:italic>\n                                 <jats:sup>\n                                    \u2212\/\u2212\n                                 <\/jats:sup> mice and littermates were conducted to distinguish the role of myeloid versus nonmyeloid <jats:italic toggle=\"yes\">Mlkl<\/jats:italic> in the Gao\u2010binge model of ALD. Ethanol\u2010induced hepatic injury, steatosis, and inflammation were exacerbated in <jats:italic toggle=\"yes\">Mlkl<\/jats:italic>\n                                 <jats:sup>\n                                    \u2212\/\u2212\n                                 <\/jats:sup>\u2192wild\u2010type (WT) mice, whereas <jats:italic toggle=\"yes\">Mlkl<\/jats:italic> deficiency in nonmyeloid cells (WT\u2192<jats:italic toggle=\"yes\">Mlkl<\/jats:italic>\n                                 <jats:sup>\n                                    \u2212\/\u2212\n                                 <\/jats:sup>) had no effect on Gao\u2010binge ethanol\u2010induced injury. Importantly, <jats:italic toggle=\"yes\">Mlkl<\/jats:italic> deficiency in myeloid cells exacerbated ethanol\u2010mediated bacterial burden and accumulation of immune cells in livers. Mechanistically, challenging macrophages with lipopolysaccharide (LPS) induced signal transducer and activator of transcription 1\u2013mediated expression and phosphorylation of MLKL, as well as translocation and oligomerization of MLKL to intracellular compartments, including phagosomes and lysosomes but not plasma membrane. Importantly, pharmacological or genetic inhibition of MLKL suppressed the phagocytic capability of primary mouse Kupffer cells (KCs) at baseline and in response to LPS with\/without ethanol as well as peripheral monocytes isolated from both healthy controls and patients with alcohol\u2010associated hepatitis. Further, <jats:italic toggle=\"yes\">in vivo<\/jats:italic> studies revealed that KCs of <jats:italic toggle=\"yes\">Mlkl<\/jats:italic>\n                                 <jats:sup>\n                                    \u2212\/\u2212\n                                 <\/jats:sup> mice phagocytosed fewer bioparticles than KCs of WT mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion:<\/jats:title>\n            <jats:p>Together, these data indicate that myeloid MLKL restricts ethanol\u2010induced liver inflammation and injury by regulating hepatic immune cell homeostasis and macrophage phagocytosis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.32612","type":"journal-article","created":{"date-parts":[[2022,6,11]],"date-time":"2022-06-11T09:19:26Z","timestamp":1654939166000},"page":"902-919","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":50,"title":["Macrophage\u2010derived MLKL in alcohol\u2010associated liver disease: Regulation of phagocytosis"],"prefix":"10.1097","volume":"77","author":[{"given":"Xiaoqin","family":"Wu","sequence":"first","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiude","family":"Fan","sequence":"additional","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan R.","family":"McMullen","sequence":"additional","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsunori","family":"Miyata","sequence":"additional","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam","family":"Kim","sequence":"additional","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vai","family":"Pathak","sequence":"additional","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, 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Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4655-5146","authenticated-orcid":false,"given":"Nicole","family":"Welch","sequence":"additional","affiliation":[{"name":"Northern Ohio Alcohol Center, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, Ohio, USA"},{"name":"Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaividhya","family":"Dasarathy","sequence":"additional","affiliation":[{"name":"Department of Family Medicine, Metro Health Medical Center, Case Western Reserve University, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela S.","family":"Allende","sequence":"additional","affiliation":[{"name":"Department of Pathology, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthur J.","family":"McCullough","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jon M.","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Biological Sciences Division and Environmental Molecular Sciences Laboratory, Pacific Northwest National Laboratory, Richland, WA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel M.","family":"Rotroff","sequence":"additional","affiliation":[{"name":"Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, Ohio, USA"},{"name":"Endocrine and Metabolism Institute, Cleveland Clinic, Cleveland, Ohio, 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