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Excessive endothelial cell (EC) activation is a critical trigger of inflammation. Extracellular vesicles (EVs) are increasingly recognized as prominent regulators of inflammatory responses. The previous study identified secretory autophagosomes (SAPs), a novel class of EVs, as a prognostic marker in ARDS, raising questions of whether and how they are involved in the pathogenesis of ARDS. Here, it is shown that inflamed macrophage\u2010derived SAPs (MSAPs) exacerbate lung injury by weakening the role of ECs as gatekeepers of immune cell transport within the lung. Bioinformatics and functional studies reveal that tRF\u20105004b is a key molecule of MSAPs in mediating endothelial activation. Mechanically, tRF\u20105004b directly interacts with the nuclear transporter KPNA2, thereby facilitating the association between KPNA2 and the transcription factor p65. This interaction enhances p65 nuclear translocation, a process implicated in EC activation. Additionally, the level of tRF\u20105004b is positively correlated with the severity of ARDS, and patients with high tRF\u20105004b levels have a poor prognosis. Overall, it is found that tRF\u20105004b\u2010enriched SAPs induce acute lung injury by promoting p65 nuclear translocation to activate ECs, suggesting that tRF\u20105004b may be a novel therapeutic target for ARDS.<\/jats:p>","DOI":"10.1002\/advs.202503014","type":"journal-article","created":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T05:56:30Z","timestamp":1750398990000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["tRF\u20105004b Enriched Secretory Autophagosomes Induce Endothelial Cell Activation to Drive Acute Respiratory Distress Syndrome"],"prefix":"10.1002","volume":"12","author":[{"given":"Xing\u2010xing","family":"Zhu","sequence":"first","affiliation":[{"name":"Jiangsu Provincial Key Laboratory of Critical Care Medicine Department of Critical Care Medicine Zhongda Hospital School of Medicine Southeast University  Nanjing Jiangsu 210009 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