{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T16:28:51Z","timestamp":1787502531076,"version":"build-2736575974"},"reference-count":48,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,1,31]],"date-time":"2025-01-31T00:00:00Z","timestamp":1738281600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,1,31]],"date-time":"2025-01-31T00:00:00Z","timestamp":1738281600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Lung ischemia reperfusion injury (LIRI) represents an evitable but significant pathologic complication post pulmonary transplantation. Dexmedetomidine (Dex) that is extensively applied as an anesthetic adjuvant in the intensive care setting has increasingly presented outstandingly protective effect on LIRI. This article concerns the elaborate role of Dex in ferroptosis after LIRI and the correlative downstream mechanism. Upon hypoxia\/reoxygenation (H\/R) in human (A549) and mouse (MLE\u201012) alveolar epithelial cells, reverse transcription\u2010quantitative PCR and western blot analysis tested nuclear receptor coactivator 4 (NCOA4) expression. CCK\u20108 kit determined cell viability. Western blot analysis and immunofluorescence assay estimated ferritinophagy. C11\u2010BODIPY 581\/591 staining, western blot analysis, assay kits and ferro\u2010orange staining appraised ferroptosis. Molecular docking technology investigated the binding affinity between Dex and nuclear factor erythroid 2\u2010related factor 2 (NRF2). Cell viability was eliminated and ferritinophagy was aggravated in A549 and MLE\u201012 cells in response to H\/R. Disturbance of NCOA4 or treatment with Dex suppressed the ferroptosis in H\/R\u2010stimulated cells. Also, Dex docked with NRF2 and upregulated NRF2 to concentration\u2010dependently obstruct NCOA4\u2010mediated ferritinophagy and ferroptosis in H\/R\u2010challenged cells. Collectively, Dex might protect against NCOA4\u2010mediated ferritinophagy through targeting NRF2, thereby alleviating ferroptosis during LIRI.<\/jats:p>","DOI":"10.1002\/jbt.70122","type":"journal-article","created":{"date-parts":[[2025,1,31]],"date-time":"2025-01-31T06:56:21Z","timestamp":1738306581000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Dexmedetomidine Blocks NCOA4\u2010Dependent Ferritinophagy to Confer Ferroptosis Resistance in Lung Ischemia Reperfusion Injury via Targeting NRF2"],"prefix":"10.1002","volume":"39","author":[{"given":"Li","family":"Qu","sequence":"first","affiliation":[{"name":"People's Hospital of Xinjiang Uygur Autonomous Region Xinjiang Clinical Research Center for Anesthesia Management Urumqi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alimujiang","family":"Simayi","sequence":"additional","affiliation":[{"name":"People's Hospital of Xinjiang Uygur 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