{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T21:47:15Z","timestamp":1792273635548,"version":"4.4.0"},"reference-count":54,"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>In obesity and type 2 diabetes mellitus, leptin promotes insulin resistance and contributes to the progression of NASH via activation of hepatic stellate cells (HSCs). However, the pathogenic mechanisms that trigger HSC activation in leptin\u2010deficient obesity are still unknown. This study aimed to determine how HSC\u2010targeting lipocalin\u20102 (LCN2) mediates the transition from simple steatosis to NASH.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results:<\/jats:title>\n            <jats:p>Male wild\u2010type (WT) and ob\/ob mice were fed a high\u2010fat diet (HFD) for 20\u2009weeks to establish an animal model of NASH with fibrosis. Ob\/ob mice were subject to caloric restriction or recombinant leptin treatment. Double knockout (DKO) mice lacking both leptin and lcn2 were also fed an HFD for 20\u2009weeks. In addition, HFD\u2010fed ob\/ob mice were treated with gadolinium trichloride to deplete Kupffer cells. The LX\u20102 human HSCs and primary HSCs from ob\/ob mice were used to investigate the effects of LCN2 on HSC activation. Serum and hepatic LCN2 expression levels were prominently increased in HFD\u2010fed ob\/ob mice compared with normal diet\u2010fed ob\/ob mice or HFD\u2010fed WT mice, and these changes were closely linked to liver fibrosis and increased hepatic \u03b1\u2010SMA\/matrix metalloproteinase 9 (MMP9)\/signal transducer and activator of transcription 3 (STAT3) protein levels. HFD\u2010fed DKO mice showed a marked reduction of \u03b1\u2010SMA protein compared with HFD\u2010fed ob\/ob mice. In particular, the colocalization of LCN2 and \u03b1\u2010SMA was increased in HSCs from HFD\u2010fed ob\/ob mice. In primary HSCs from ob\/ob mice, exogenous LCN2 treatment induced HSC activation and MMP9 secretion. By contrast, LCN2 receptor 24p3R deficiency or a STAT3 inhibitor reduced the activation and migration of primary HSCs.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>LCN2 acts as a key mediator of HSC activation in leptin\u2010deficient obesity via \u03b1\u2010SMA\/MMP9\/STAT3 signaling, thereby exacerbating NASH.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.32569","type":"journal-article","created":{"date-parts":[[2022,5,13]],"date-time":"2022-05-13T03:45:00Z","timestamp":1652413500000},"page":"888-901","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":76,"title":["Lipocalin\u20102 activates hepatic stellate cells and promotes nonalcoholic steatohepatitis in high\u2010fat diet\u2013fed Ob\/Ob mice"],"prefix":"10.1097","volume":"77","author":[{"given":"Kyung Eun","family":"Kim","sequence":"first","affiliation":[{"name":"Department of 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Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye Min","family":"Jang","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu Jeong","family":"Ahn","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyeong Seok","family":"An","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jong Youl","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meong Cheol","family":"Shin","sequence":"additional","affiliation":[{"name":"College of Pharmacy, Research Institute of Pharmaceutical Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soo Kyoung","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Won Gi","family":"Yoo","sequence":"additional","affiliation":[{"name":"Department of Parasitology and Tropical Medicine, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Won Ho","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Diseases, Center for Biomedical Sciences, Korea National Institute of Health, Cheongju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gu Seob","family":"Roh","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju, Republic of 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