{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T15:11:29Z","timestamp":1792681889550,"version":"4.5.0"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2021,4,27]],"date-time":"2021-04-27T00:00:00Z","timestamp":1619481600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2021,4,27]],"date-time":"2021-04-27T00:00:00Z","timestamp":1619481600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background ands Aims<\/jats:title>\n                    <jats:p>NAFLD is associated with elevation of many cytokines, particularly IL\u20106; however, the role of IL\u20106 in NAFLD remains obscure. The aim of this study was to examine how myeloid\u2010specific IL\u20106 signaling affects NAFLD by the regulation of antifibrotic microRNA\u2010223 (miR\u2010223) in myeloid cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results<\/jats:title>\n                    <jats:p>\n                      Patients with NAFLD or NASH and healthy controls were recruited, and serum IL\u20106 and soluble IL\u20106 receptor \u03b1 (sIL\u20106R\u03b1) were measured. Compared to controls, serum IL\u20106 and sIL\u20106R\u03b1 levels were elevated in NAFLD\/NASH patients. IL\u20106 levels correlated positively with the number of circulating leukocytes and monocytes. The role of IL\u20106 in NAFLD was investigated in\n                      <jats:italic toggle=\"yes\">Il6<\/jats:italic>\n                      knockout (KO) and\n                      <jats:italic toggle=\"yes\">Il6<\/jats:italic>\n                      receptor A (\n                      <jats:italic toggle=\"yes\">Il6ra<\/jats:italic>\n                      ) conditional KO mice after high\u2010fat diet (HFD) feeding. HFD\u2010fed\n                      <jats:italic toggle=\"yes\">Il6<\/jats:italic>\n                      KO mice had worse liver injury and fibrosis, but less inflammation, compared to wild\u2010type mice. Hepatocyte\u2010specific\n                      <jats:italic toggle=\"yes\">Il6ra<\/jats:italic>\n                      KO mice had more steatosis and liver injury, whereas myeloid\u2010specific\n                      <jats:italic toggle=\"yes\">Il6ra<\/jats:italic>\n                      KO mice had a lower number of hepatic infiltrating macrophages (IMs) and neutrophils with increased cell death of these cells, but greater liver fibrosis (LF), than WT mice. Mechanistically, the increased LF in HFD\u2010fed, myeloid\u2010specific\n                      <jats:italic toggle=\"yes\">Il6ra<\/jats:italic>\n                      KO mice was attributable to the reduction of antifibrotic miR\u2010223 and subsequent up\u2010regulation of the miR\u2010223 target gene, transcriptional activator with PDZ\u2010binding motif (TAZ), a well\u2010known factor to promote NASH fibrosis.\n                      <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                      , IL\u20106 treatment up\u2010regulated exosome biogenesis\u2010related genes and subsequently promoted macrophages to release miR\u2010223\u2010enriched exosomes that were able to reduce profibrotic TAZ expression in hepatocytes by exosomal transfer. Finally, serum IL\u20106 and miR\u2010223 levels were elevated and correlated with each other in NAFLD patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Myeloid\u2010specific IL\u20106 signaling inhibits LF through exosomal transfer of antifibrotic miR\u2010223 into hepatocytes, providing therapeutic targets for NAFLD therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.31658","type":"journal-article","created":{"date-parts":[[2020,11,25]],"date-time":"2020-11-25T02:44:17Z","timestamp":1606272257000},"page":"116-132","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":211,"title":["Myeloid\u2010Cell\u2013Specific IL\u20106 Signaling Promotes MicroRNA\u2010223\u2010Enriched Exosome Production to Attenuate NAFLD\u2010Associated Fibrosis"],"prefix":"10.1097","volume":"74","author":[{"given":"Xin","family":"Hou","sequence":"first","affiliation":[{"name":"Anhui Provincial Laboratory of Microbiology and Parasitology,School of Basic Medical Sciences,Anhui Medical University,Hefei,China"},{"name":"Laboratory of Liver Diseases,National Institute on Alcohol Abuse and Alcoholism,National Institutes of Health,Bethesda,MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shi","family":"Yin","sequence":"additional","affiliation":[{"name":"Laboratory of Liver Diseases,National Institute on Alcohol Abuse and Alcoholism,National Institutes of Health,Bethesda,MD"},{"name":"Department of Geriatrics,Affiliated Provincial Hospital of Anhui Medical University,Hefei,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruixue","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Oncology,the First Affiliated Hospital of Anhui Medical 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