{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T03:28:51Z","timestamp":1779334131189,"version":"3.51.4"},"reference-count":44,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,10,7]],"date-time":"2025-10-07T00:00:00Z","timestamp":1759795200000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pulm. circ."],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Mechanical ventilation (MV), though life\u2010saving in acute respiratory distress syndrome (ARDS), can cause ventilator\u2010induced lung injury (VILI). MicroRNA\u201024 (miR\u201024) has been implicated in regulating inflammation and apoptosis, but its role in VILI remains unexplored. Therefore, our study aimed to explore the role of mechanism of miR\u201024 in VILI. MiR\u201024 expression was analyzed in MV\u2010induced ARDS rat models (GSE57223), plasma from ARDS patients, and cyclic stretch (CS)\u2010treated alveolar epithelial cells. Functional studies included intratracheal delivery of miR\u201024\u2010agomir in rats with VILI and transfection of miR\u201024 mimic in CS\u2010exposed cells. Inflammatory cytokines, oxidative stress markers, apoptosis, and mitochondrial dysfunction were assessed using ELISA, RT\u2010qPCR, TUNEL, JC\u20101 staining, and ATP assays. BOK was identified as a target of miR\u201024 via bioinformatics, luciferase reporter, and RNA pull\u2010down assays. Rescue experiments using BOK overexpression vectors (pcDNA3.1\/BOK) were conducted in both models to confirm functional interaction. MiR\u201024 was significantly downregulated in ARDS patients and VILI models and positively correlated with oxygenation index. Overexpression of miR\u201024 attenuated MV\u2010 and CS\u2010induced inflammation, oxidative damage, and mitochondrial apoptosis dysfunction. BOK was confirmed as a direct target of miR\u201024; its expression was upregulated in ARDS and VILI and inversely correlated with miR\u201024 levels. Silencing of BOK attenuated MV\u2010induced inflammation, oxidative damage, and apoptosis in rats. Importantly, BOK overexpression reversed the protective effects of miR\u201024 both in vivo and in vitro, confirming its role as a key downstream effector. Receiver operating characteristic (ROC) analysis showed that miR\u201024 had good diagnostic potential (AUC\u2009=\u20090.834). Overall, MiR\u201024 protects against MV\u2010induced lung injury by targeting BOK and modulating key injury pathways. The miR\u201024\/BOK axis offers a promising therapeutic avenue for ARDS\u2010associated VILI.<\/jats:p>","DOI":"10.1002\/pul2.70171","type":"journal-article","created":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T04:39:57Z","timestamp":1759898397000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["MiR\u201024 Attenuates Oxidative Stress and Mitochondrial Apoptosis in Ventilator\u2010Induced Lung Injury by Targeting Bcl\u20102\u2010related Ovarian Killer"],"prefix":"10.1002","volume":"15","author":[{"given":"Wenbo","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Critical Care Medicine Changzhou Jintan First People's Hospital Changzhou Jiangsu China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wenjiao","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine Changzhou Jintan First People's Hospital Changzhou Jiangsu 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