{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:01:01Z","timestamp":1790640061340,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T00:00:00Z","timestamp":1790553600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T00:00:00Z","timestamp":1790553600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["22K16549"],"award-info":[{"award-number":["22K16549"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Metabolic dysfunction\u2010associated steatotic liver disease (MASLD) affects approximately 25% of the global population and is a major health concern. Liver sinusoidal endothelial cells (LSECs) undergo morphological and functional alterations during MASLD progression, resulting in endotheliopathy characterized by pro\u2010inflammatory phenotypes. We hypothesize that lipotoxicity synergistically exacerbates LSEC dysfunction in MASLD via IL\u20106 trans\u2010signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Human adipocytes were treated with palmitic acid (PA). Human LSECs were treated with PA and the IL\u20106\/soluble IL\u20106 receptor (sIL\u20106R) complex. Western blotting, qRT\u2010PCR, RNA sequencing, transwell assays, and immunofluorescence were performed to examine inflammatory responses. MASLD model mice were established using a choline\u2010deficient, L\u2010amino acid\u2010defined, high\u2010fat diet (CDAHFD) to validate the in\u00a0vivo results. Alterations in LSEC morphology were examined by western blotting, histology, and electron microscopy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>PA promoted IL\u20106 secretion from adipocytes. In LSECs, PA increased NF\u03baB phosphorylation, whereas co\u2010stimulation with PA and IL\u20106\/sIL\u20106R complex synergistically enhanced activator of transcription 3 (STAT3) phosphorylation and upregulated inflammatory cytokines, chemokines, and adhesion molecules, including VCAM1. Furthermore, RNA sequencing showed concurrent NF\u03baB and Janus kinase (JAK)\/STAT pathway activation. This synergistic effect promoted neutrophil migration and VCAM1 expression under in\u00a0vitro conditions. In the MASLD mouse model, hepatic IL\u20106 expression was elevated, accompanied by steatosis, increased transaminase levels, and inflammatory cell infiltration, along with increased VCAM1 expression and sinusoidal capillarization characterized by upregulated CD34 and downregulated CD32b and LYVE\u20101.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Lipotoxicity\u2010amplified IL\u20106 trans\u2010signaling synergistically exacerbates LSEC endotheliopathy and promotes leukocyte recruitment and liver injury, contributing to MASLD progression and providing novel insights into its pathogenesis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jgh.70782","type":"journal-article","created":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T23:30:50Z","timestamp":1790638250000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Lipotoxicity Amplifies IL\u20106 Trans\u2010Signaling in Sinusoidal Endothelial Cells to Promote Endotheliopathy and Liver Injury"],"prefix":"10.1111","author":[{"given":"Yasuhiko","family":"Ueda","sequence":"first","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nao","family":"Kawaguchi","sequence":"additional","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4897-5707","authenticated-orcid":false,"given":"Yosuke","family":"Inomata","sequence":"additional","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Arima","sequence":"additional","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9585-4118","authenticated-orcid":false,"given":"Mitsuaki","family":"Ishida","sequence":"additional","affiliation":[{"name":"Department of Pathology Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuko","family":"Ito","sequence":"additional","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang\u2010Woong","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0648-1370","authenticated-orcid":false,"given":"Kohei","family":"Taniguchi","sequence":"additional","affiliation":[{"name":"Department of General and Gastroenterological Surgery Osaka Medical and Pharmaceutical University  Osaka Japan"},{"name":"Center for Research &amp; Development, Division of Translational Research Osaka Medical and Pharmaceutical University  Osaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,28]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"crossref","first-page":"314","DOI":"10.1007\/s00018-023-04966-7","article-title":"Liver Endothelial Cells in NAFLD and Transition to NASH and HCC","volume":"80","author":"Velliou R. 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