{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,1]],"date-time":"2026-11-01T16:07:41Z","timestamp":1793549261429,"version":"4.5.0"},"reference-count":42,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2023,4,1]],"date-time":"2023-04-01T00:00:00Z","timestamp":1680307200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82060372"],"award-info":[{"award-number":["82060372"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Alveolar echinococcosis (AE) is a lethal helminthic liver disease caused by persistent infection with\n                    <jats:italic>Echinococcus multilocularis<\/jats:italic>\n                    (\n                    <jats:italic>E. multilocularis<\/jats:italic>\n                    ). Although more and more attention has been paid to the macrophages in\n                    <jats:italic>E. multilocularis<\/jats:italic>\n                    infection, the mechanism of macrophage polarization, a critical player in liver immunity, is seldom studied. NOTCH signaling is involved in cell survival and macrophage\u2010mediated inflammation, but the role of NOTCH signaling in AE has been equally elusive. In this study, liver tissue samples from AE patients were collected and an\n                    <jats:italic>E. multilocularis<\/jats:italic>\n                    infected mouse model with or without blocking NOTCH signaling was established to analyze the NOTCH signaling, fibrotic and inflammatory response of the liver after\n                    <jats:italic>E. multilocularis<\/jats:italic>\n                    infection. Changes in polarization and origin of hepatic macrophages were analyzed by flow cytometry. In vitro qRT\u2010PCR and Western blot assays were performed to analyze key receptors and ligands in NOTCH signaling. Our data demonstrated that hepatic fibrosis develops after AE, and the overall blockade of NOTCH signaling caused by DAPT treatment exacerbates the levels of hepatic fibrosis and alters the polarization and origin of hepatic macrophages. Blocking NOTCH signaling in macrophages after\n                    <jats:italic>E. multilocularis<\/jats:italic>\n                    infection downregulates M1 and upregulates M2 expression. The downregulation of NTCH3 and DLL\u20103 in the NOTCH signaling pathway is significant. Therefore, NOTCH3\/DLL3 may be the key pathway in NOTCH signaling regulating macrophage polarization affecting fibrosis caused by AE.\n                  <\/jats:p>","DOI":"10.1096\/fj.202202033r","type":"journal-article","created":{"date-parts":[[2023,4,1]],"date-time":"2023-04-01T09:35:40Z","timestamp":1680341740000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["<scp>NOTCH<\/scp>\n                    signaling inhibition after\n                    <scp>DAPT<\/scp>\n                    treatment exacerbates alveolar echinococcosis hepatic fibrosis by blocking\n                    <scp>M1<\/scp>\n                    and enhancing\n                    <scp>M2<\/scp>\n                    polarization"],"prefix":"10.1096","volume":"37","author":[{"given":"Bin","family":"Li","sequence":"first","affiliation":[{"name":"State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Laboratory Center Tumor Hospital Affiliated to Xinjiang Medical University  Urumqi Xinjiang 830011 P.R. 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