{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T20:24:19Z","timestamp":1782505459336,"version":"3.54.5"},"reference-count":34,"publisher":"Wiley","issue":"20","license":[{"start":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T00:00:00Z","timestamp":1770163200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T00:00:00Z","timestamp":1770163200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100002858","name":"China Postdoctoral Science Foundation","doi-asserted-by":"publisher","award":["2022M723298"],"award-info":[{"award-number":["2022M723298"]}],"id":[{"id":"10.13039\/501100002858","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Liver fibrosis, driven by excessive collagen synthesis following hepatic injury, poses a significant health challenge. SLC39A13\/ZIP13, a recently characterized intracellular iron transporter, is shown to provide iron to the ER\/Golgi to help catalyze procollagen hydroxylation during collagen maturation. Here, we investigate whether ZIP13 plays a role during hepatic fibrogenesis modeled by CCl\n                    <jats:sub>4<\/jats:sub>\n                    stress or other inducers. ZIP13 expression is induced during liver fibrosis. Germline disruption of\n                    <jats:italic>Zip13<\/jats:italic>\n                    dramatically reduces fibrosis. Surprisingly, these mice do not benefit from ZIP13 loss after CCl\n                    <jats:sub>4<\/jats:sub>\n                    challenge; instead, they are more susceptible to CCl\n                    <jats:sub>4<\/jats:sub>\n                    toxicity even with substantially less fibrosis development. This elevated vulnerability turns out to be a consequence of ferroptosis in the hepatocyte due to increased cytosolic iron after ZIP13 loss. Tissue\u2010specific knockout (KO) reveals that hepatic stellate cell (HSC) KO of\n                    <jats:italic>Zip13<\/jats:italic>\n                    attenuates liver fibrosis progression without adverse effects. Leveraging these findings, HSC\u2010targeted delivery of\n                    <jats:italic>Zip13<\/jats:italic>\n                    \u2010siRNA demonstrates robust efficacy and safety in preclinical fibrosis models. These results provide critical insights into the complex role of iron in liver fibrosis, and indicate that targeting iron homeostasis via ZIP13 in the HSC may be effective to mitigate fibrogenesis by simultaneously suppressing the synthesis of multiple kinds of collagen while minimizing possible side effects.\n                  <\/jats:p>","DOI":"10.1002\/advs.202516446","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T15:31:21Z","timestamp":1770219081000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The Regulatory Role of Iron Transporter SLC39A13 in Liver Fibrosis"],"prefix":"10.1002","volume":"13","author":[{"given":"Shanshan","family":"Guo","sequence":"first","affiliation":[{"name":"Faculty of Synthetic Biology Shenzhen University of Advanced Technology  Shenzhen China"},{"name":"Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences  Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yalin","family":"Wang","sequence":"additional","affiliation":[{"name":"Faculty of Synthetic Biology Shenzhen University of Advanced Technology  Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binyu","family":"Lu","sequence":"additional","affiliation":[{"name":"Faculty of Synthetic Biology Shenzhen University of Advanced Technology  Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Zhang","sequence":"additional","affiliation":[{"name":"Faculty of Synthetic Biology Shenzhen University of Advanced Technology  Shenzhen China"},{"name":"Key Laboratory of Quantitative Synthetic Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences  Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Frazer","sequence":"additional","affiliation":[{"name":"Molecular Nutrition Laboratory QIMR Berghofer Medical Research Institute Herston Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6585-9284","authenticated-orcid":false,"given":"Bing","family":"Zhou","sequence":"additional","affiliation":[{"name":"Faculty of Synthetic Biology Shenzhen University of Advanced Technology  Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,2,4]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12967-023-04690-7"},{"key":"e_1_2_11_3_1","first-page":"68","article-title":"Liver Fibrosis: Direct Antifibrotic Agents and Targeted Therapies","volume":"435","author":"Schuppan D.","year":"2018","journal-title":"Matrix 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