{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T07:09:54Z","timestamp":1790060994910,"version":"4.0.1"},"reference-count":41,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100012226","name":"Fundamental Research Funds for the Central Universities","doi-asserted-by":"publisher","award":["2042025YXB019"],"award-info":[{"award-number":["2042025YXB019"]}],"id":[{"id":"10.13039\/501100012226","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MedComm"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Ischemia\/reperfusion (I\/R)\u2010induced acute lung injury (ALI) is a severe clinical syndrome characterized by alveolar epithelial damage, oxidative stress, and acute respiratory failure, but the epitranscriptomic mechanisms linking N6\u2010methyladenosine (m6A) modification to ferroptosis remain unclear. Clinical profiling of end\u2010stage acute respiratory distress syndrome (ARDS) patients showed hyperinflammation, reflected by elevated C\u2010reactive protein and procalcitonin, coagulopathy with abnormal D\u2010dimer levels, and severely impaired gas exchange. Reanalysis of a public murine single\u2010cell RNA sequencing dataset revealed enrichment of RNA methylation\u2010, ubiquitination\u2010, and ferroptosis\u2010related programs in injured lung epithelial cells. Integrated methylated RNA immunoprecipitation sequencing and RNA sequencing of I\/R\u2010injured mouse lungs further identified methyltransferase\u2010like 14 (METTL14) and YTH N6\u2010methyladenosine RNA\u2010binding protein 1 (YTHDF1) as candidate m6A regulators. Human ARDS tissues and mouse I\/R lungs confirmed increased METTL14, ubiquitin\u2010specific peptidase 30 (USP30), and nuclear receptor coactivator 4 (NCOA4) expression. Mechanistically, METTL14\u2010mediated m6A modification enhanced USP30 expression through YTHDF1 recognition, whereas USP30 stabilized NCOA4 by reducing K48\u2010linked polyubiquitination. Stabilized NCOA4 promoted ferritinophagy, Fe\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    accumulation, lipid peroxidation, and epithelial ferroptosis. These findings identify a METTL14\/YTHDF1\u2010USP30\u2010NCOA4 axis as a potential therapeutic target for ferroptosis\u2010driven I\/R\u2010induced ALI.\n                  <\/jats:p>","DOI":"10.1002\/mco2.70959","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T07:04:23Z","timestamp":1787900663000},"source":"Crossref","is-referenced-by-count":0,"title":["METTL14\u2010Mediated N6\u2010Methyladenosine Exacerbates Acute Lung Injury via USP30\/NCOA4\u2010Dependent Ferroptosis"],"prefix":"10.1002","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6590-8963","authenticated-orcid":false,"given":"Aming","family":"Sang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Zhongnan Hospital of Wuhan University  Wuhan Hubei China"},{"name":"Hubei Provincial Engineering Research Center of Minimally Invasive Cardiovascular Surgery  Wuhan Hubei 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