{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T23:17:25Z","timestamp":1793229445298,"version":"4.5.0"},"reference-count":65,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,7,21]],"date-time":"2022-07-21T00:00:00Z","timestamp":1658361600000},"content-version":"vor","delay-in-days":201,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100008233","name":"School of Medicine, Shanghai Jiao Tong University","doi-asserted-by":"publisher","award":["DLY201803"],"award-info":[{"award-number":["DLY201803"]}],"id":[{"id":"10.13039\/501100008233","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81772040"],"award-info":[{"award-number":["81772040"]}],"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":["81772107"],"award-info":[{"award-number":["81772107"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:p>\n                    <jats:italic>Background<\/jats:italic>\n                    . Ferroptosis is a nonapoptotic form of programmed cell death, which may be related to the occurrence and development of sepsis\u2010induced acute respiratory distress syndrome (ARDS)\/acute lung injury (ALI). Mucin 1 (MUC1) is a kind of macromolecule transmembrane glycoprotein. Previous studies have shown that MUC1 could relieve ALI in sepsis and predict whether sepsis patients would develop into ARDS. However, the role of MUC1 in the ferroptosis of sepsis\u2010induced ALI\/ARDS remains unclear.\n                    <jats:italic>Materials and Methods<\/jats:italic>\n                    . Sera samples from 50 patients with sepsis\/septic shock were used to detect iron metabolism\u2010related markers. Western blot and qRT\u2010PCR were conducted to detect the expression levels of ferroptosis\u2010related genes. Enzyme\u2010linked immunosorbent assay (ELISA) was performed to evaluate inflammatory factors. Transmission electron microscopy (TEM) was used to assess morphological changes of cells.\n                    <jats:italic>Results<\/jats:italic>\n                    . The results showed that the iron metabolism\u2010related indicators in sepsis\u2010induced ARDS patients changed significantly, suggesting the iron metabolism disorder. The expression levels of ferroptosis\u2010related genes in lung tissues of sepsis had marked changes, and the lipid peroxidation levels increased, while Ferrostatin\u20101 (Fer\u20101) could reverse the above results, which confirmed the occurrence of ferroptosis. In terms of mechanism studies, inhibition of MUC1 dimerization could increase the expression level of Keap1, reduce the phosphorylation level of GSK3\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , inhibit the entry of Nrf2 into the nucleus, further inhibit the expression level of GPX4, enhance the lipid peroxidation level of lung tissues, trigger ferroptosis, and aggravate lung injury. Besides, inhibiting MUC1 reversed the alleviating effect of vitamin E on ALI caused by sepsis, increased the aggregation of inflammatory cells in lung tissues, and aggravated alveolar injury and edema.\n                    <jats:italic>Conclusions<\/jats:italic>\n                    . Our study was the first to explore the changes of iron metabolism indicators in ALI\/ARDS of sepsis, clarify the important role of ferroptosis in ALI\/ARDS induced by sepsis, and reveal the effects and specific mechanisms of MUC1 in regulating ferroptosis, as well as the sensitization on vitamin E.\n                  <\/jats:p>","DOI":"10.1155\/2022\/2405943","type":"journal-article","created":{"date-parts":[[2022,7,21]],"date-time":"2022-07-21T18:50:10Z","timestamp":1658429410000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Mucin 1 Inhibits Ferroptosis and Sensitizes Vitamin E to Alleviate Sepsis\u2010Induced Acute Lung Injury through GSK3\n                    <i>\u03b2<\/i>\n                    \/Keap1\u2010Nrf2\u2010GPX4 Pathway"],"prefix":"10.1155","volume":"2022","author":[{"given":"Yu-Ming","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9502-8126","authenticated-orcid":false,"given":"Fang-Chen","family":"Gong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xing","family":"Qi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan-Jun","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiang-Tao","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2688-8736","authenticated-orcid":false,"given":"Ying","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi-Tao","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Qing-Ye","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"En-Qiang","family":"Mao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7835-6080","authenticated-orcid":false,"given":"Er-Zhen","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2022,7,21]]},"reference":[{"key":"e_1_2_13_1_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2016.0287"},{"key":"e_1_2_13_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcna.2020.02.011"},{"key":"e_1_2_13_3_2","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.201504-0781OC"},{"key":"e_1_2_13_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0908610"},{"key":"e_1_2_13_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0199-3"},{"key":"e_1_2_13_6_2","doi-asserted-by":"publisher","DOI":"10.21037\/atm.2016.08.59"},{"key":"e_1_2_13_7_2","doi-asserted-by":"publisher","DOI":"10.1080\/14728222.2021.1897107"},{"key":"e_1_2_13_8_2","doi-asserted-by":"publisher","DOI":"10.4046\/trd.2016.79.2.53"},{"key":"e_1_2_13_9_2","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e31816fc2c0"},{"key":"e_1_2_13_10_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1608077"},{"key":"e_1_2_13_11_2","first-page":"352","article-title":"Acute 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