{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T11:53:03Z","timestamp":1792583583100,"version":"4.5.0"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2024,3,15]],"date-time":"2024-03-15T00:00:00Z","timestamp":1710460800000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81930058"],"award-info":[{"award-number":["81930058"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82341032"],"award-info":[{"award-number":["82341032"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82072154"],"award-info":[{"award-number":["82072154"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Extracellular Vesicle"],"published-print":{"date-parts":[[2024,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Acute lung injury (ALI)\/acute respiratory distress syndrome (ARDS) is a common life\u2010threatening syndrome with no effective pharmacotherapy. Sepsis\u2010related ARDS is the main type of ARDS and is more fatal than other types. Extracellular vesicles (EVs) are considered novel mediators in the development of inflammatory diseases. Our previous research suggested that endothelial cell\u2010derived EVs (EC\u2010EVs) play a crucial role in ALI\/ARDS development, but the mechanism remains largely unknown. Here, we demonstrated that the number of circulating EC\u2010EVs was increased in sepsis, exacerbating lung injury by targeting monocytes and reprogramming them towards proinflammatory macrophages. Bioinformatics analysis and further mechanistic studies revealed that vascular cell adhesion molecule 1 (VCAM1), overexpressed on EC\u2010EVs during sepsis, activated the NF\u2010\u03baB pathway by interacting with integrin subunit alpha 4 (ITGA4) on the monocyte surface, rather than the tissue resident macrophage surface, thereby regulating monocyte differentiation. This effect could be attenuated by decreasing VCAM1 levels in EC\u2010EVs or blocking ITGA4 on monocytes. Furthermore, the number of VCAM1\n                    <jats:sup>+<\/jats:sup>\n                    EC\u2010EVs was significantly increased in patients with sepsis\u2010related ARDS. These findings not only shed light on a previously unidentified mechanism underling sepsis\u2010related ALI\/ARDS, but also provide potential novel targets and strategies for its precise treatment.\n                  <\/jats:p>","DOI":"10.1002\/jev2.12423","type":"journal-article","created":{"date-parts":[[2024,3,16]],"date-time":"2024-03-16T02:36:26Z","timestamp":1710556586000},"source":"Crossref","is-referenced-by-count":87,"title":["Endothelial cell\u2010derived extracellular vesicles expressing surface VCAM1 promote sepsis\u2010related acute lung injury by targeting and reprogramming monocytes"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-8866-8610","authenticated-orcid":false,"given":"Lu","family":"Wang","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 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