{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T13:28:21Z","timestamp":1773926901885,"version":"3.50.1"},"reference-count":33,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:00:00Z","timestamp":1772496000000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"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":[[2026,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Sepsis\u2010associated acute lung injury (SALI) is a severe complication of sepsis, characterized by excessive inflammation and high mortality. Ferroptosis, an iron\u2010dependent form of cell death, has been implicated in the pathogenesis of SALI. This study investigates the role of lncRNA KCNJ2\u2010AS1 in SALI, focusing on its regulation of ferroptosis and inflammatory responses. Differential expression analysis identified KCNJ2\u2010AS1 as upregulated in sepsis patients. KCNJ2\u2010AS1 expression was measured by RT\u2010qPCR in 115 SALI patients and controls. Its association with inflammatory markers and prognostic value for 28\u2010day prognosis were further evaluated. The effects of KCNJ2\u2010AS1 on ferroptosis markers and ROS levels were examined in HPAEpiC cells using in vitro experiments. The involvement of the KCNJ2\u2010AS1\/miR\u2010212\u20103p\/EGR1 axis was explored using dual\u2010luciferase assays and functional studies. KCNJ2\u2010AS1 was overexpressed in SALI patients, correlating with increased inflammatory cytokines and reduced survival. In vitro, KCNJ2\u2010AS1 induced ferroptosis, increasing ROS and Fe\u00b2\u207a levels while downregulating GPX4 and upregulating ACSL4. Ferroptosis inhibition Fer\u20101 reversed these effects. Additionally, KCNJ2\u2010AS1 regulated the miR\u2010212\u20103p\/EGR1 axis, modulating inflammation and ferroptosis in the LPS\u2010induced SALI model. KCNJ2\u2010AS1 may promote SALI pathogenesis by regulating ferroptosis and inflammation via the miR\u2010212\u20103p\/EGR1 axis, emerging as a potential biomarker and therapeutic target.<\/jats:p>","DOI":"10.1002\/jbt.70712","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T23:10:55Z","timestamp":1773011455000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["KCNJ2\u2010AS1 Drives Inflammation and Ferroptosis via the miR\u2010212\u20103p\/EGR1 Axis in Sepsis\u2010Associated Acute Lung Injury"],"prefix":"10.1002","volume":"40","author":[{"given":"Yiping","family":"Pan","sequence":"first","affiliation":[{"name":"Department of Intensive Care Unit The First Affiliated Hospital of Guangxi Medical University  Nanning Guangxi China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jie","family":"Lai","sequence":"additional","affiliation":[{"name":"Department of Intensive 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