{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,20]],"date-time":"2026-03-20T04:06:23Z","timestamp":1773979583033,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T00:00:00Z","timestamp":1742169600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100012166","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","award":["2024YFA1107402"],"award-info":[{"award-number":["2024YFA1107402"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32070724"],"award-info":[{"award-number":["32070724"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32471206"],"award-info":[{"award-number":["32471206"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82000582"],"award-info":[{"award-number":["82000582"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82070008"],"award-info":[{"award-number":["82070008"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FEBS Journal"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:p>\n                    Several liver diseases have been associated with the Tudor staphylococcal nuclease (Tudor\u2010SN) protein. Our previous results demonstrated that, in comparison to wild\u2010type (WT) mice, systemic overexpression of\n                    <jats:italic>Tudor\u2010SN<\/jats:italic>\n                    in transgenic (Tg) mice (Tudor\u2010SN\u2010Tg) ameliorates obesity\u2010induced insulin resistance and hepatic steatosis. In this study, we observed an inverse correlation in the expression levels of Tudor\u2010SN and profibrogenic factors, such as alpha\u2010smooth muscle actin (\u03b1\u2010SMA) and collagen alpha\u20101(I) chain (COL1A1), in liver tissue samples between Tudor\u2010SN\u2010Tg and WT mice. The correlation was further validated in hepatic fibrotic tissues from patients with cirrhosis and fibrosis. Utilizing a carbon tetrachloride (CCl\n                    <jats:sub>4<\/jats:sub>\n                    )\u2010induced hepatic fibrosis model, we observed that Tudor\u2010SN attenuated hepatic fibrosis in mice.\n                    <jats:italic>Tudor\u2010SN<\/jats:italic>\n                    was abundantly expressed in hepatic stellate cells (HSCs). In the Tudor\u2010SN\u2010Tg group, primary HSCs showed stellate\u2010like morphology as well as reduced\n                    <jats:italic>in vitro<\/jats:italic>\n                    proliferation and chemotactic ability compared to the WT group. Pseudotime series analysis of HSCs further showed the role of Tudor\u2010SN during the dynamic evolution of HSC activation. Reduced Tudor\u2010SN expression facilitated the\n                    <jats:italic>in vitro<\/jats:italic>\n                    activation of LX\u20102 cells. Furthermore, primary HSC cells from WT and Tudor\u2010SN knockout (KO) mice were isolated for RNA\u2010sequencing analysis. The findings suggested that Tudor\u2010SN may regulate the activation of primary HSCs by influencing lipid metabolism, translation initiation, immune response, and the extracellular matrix. In summary, we identified Tudor\u2010SN as a newly identified regulator involved in the transition of quiescent HSCs to activated states, shedding light on the antifibrotic impact of Tudor\u2010SN expression in the development of hepatic fibrosis.\n                  <\/jats:p>","DOI":"10.1111\/febs.70073","type":"journal-article","created":{"date-parts":[[2025,3,18]],"date-time":"2025-03-18T02:13:47Z","timestamp":1742264027000},"page":"3545-3564","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Tudor staphylococcal nuclease (Tudor\u2010\n                    <scp>SN<\/scp>\n                    ) regulates activation of quiescent hepatic stellate cells"],"prefix":"10.1111","volume":"292","author":[{"given":"Baoxin","family":"Qian","sequence":"first","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co\u2010sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education) Tianjin Medical University  China"},{"name":"Department of Biochemistry and Molecular Biology, School of Basic Medical Science Tianjin Medical University  China"},{"name":"Department of Immunology, School of Basic Medical Science Tianjin Medical University  China"},{"name":"Department of Gastroenterology and Hepatology, Nankai University Affinity the Third Central Hospital, Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center Tianjin Institute of Hepatobiliary Disease  China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Zhao","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Experimental Hematology, Key Laboratory of 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