{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T20:46:41Z","timestamp":1792183601872,"version":"4.4.0"},"reference-count":42,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T00:00:00Z","timestamp":1765584000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T00:00:00Z","timestamp":1765584000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82272421"],"award-info":[{"award-number":["82272421"]}],"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":["82570746"],"award-info":[{"award-number":["82570746"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background &amp; Aims<\/jats:title>\n                    <jats:p>Liver fibrosis significantly burdens global health, and increased protein synthesis during hepatic stellate cell (HSC) activation plays a crucial role in its progression. Ribosome is the site of protein synthesis. RNA polymerase I (Pol I) is a protein that regulates the transcription of ribosomal DNA (rDNA) genes into ribosomal RNA (rRNA) in ribosomal biogenesis. Therefore, we investigated the role and mechanism of Pol I\u2010regulated ribosome biogenesis in HSCs activation and liver fibrosis progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Initially, we assessed the expression levels of Pol I in the serum of patients diagnosed with liver fibrosis. Then, we assessed Pol I\u2010regulated ribosome biogenesis levels in mouse models of metabolic dysfunction\u2010associated steatohepatitis (MASH) and carbon tetrachloride (CCl\n                      <jats:sub>4<\/jats:sub>\n                      ). Finally, we employed overexpression or knockdown of the Pol I gene in LX2 cells or utilised the Pol I inhibitor CX\u20105461 in\u00a0vivo and in\u00a0vitro, assessing the levels of ribosome biogenesis and HSCs activation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pol I levels were elevated in the serum of patients with liver fibrosis. Additionally, Pol I\u2010regulated ribosome biogenesis levels were significantly increased in both MASH and CCl\n                      <jats:sub>4<\/jats:sub>\n                      mouse models, as well as in HSCs activated by transforming growth factor beta 1 (TGF\u03b21). The overexpression of Pol I was found to enhance the activation of HSCs and promote ribosome biogenesis, while the knockdown of Pol I or the inhibitor CX\u20105461 inhibited these processes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Pol I\u2010regulated ribosome biogenesis is significantly increased during HSCs activation and liver fibrosis progression. Pol I may serve as a potential target for the diagnosis and treatment of liver fibrosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.70478","type":"journal-article","created":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T09:25:44Z","timestamp":1765617944000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Targeting\n                    <scp>RNA<\/scp>\n                    Polymerase I Inhibits Ribosome Biogenesis to Block Liver Fibrosis Progression"],"prefix":"10.1111","volume":"46","author":[{"given":"Wei","family":"Luo","sequence":"first","affiliation":[{"name":"Changzhou Key Laboratory of Exosome Basics and Translational Applications Wujin Hospital Affiliated With Jiangsu University  Changzhou China"},{"name":"Wujin Institute of Molecular Diagnostics and Precision Cancer Medicine of Jiangsu University  Changzhou 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