{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T15:35:55Z","timestamp":1791041755992,"version":"4.1.0"},"reference-count":37,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,5,6]],"date-time":"2025-05-06T00:00:00Z","timestamp":1746489600000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Respiratory J"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Intercellular cell adhesion molecule 1 (ICAM1) has been confirmed to be abnormally expressed in acute respiratory distress syndrome (ARDS) patients. However, its role and mechanism in pediatric ARDS process need further revealed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Serum samples were selected from pediatric ARDS patients and age\u2010matched healthy individuals. Lipopolysaccharide (LPS)\u2010induced human pulmonary microvascular endothelial cells (HPMECs) were used to mimic ARDS cell models. Cell proliferation and apoptosis were tested by cell counting kit 8 assay, EdU assay, and flow cytometry. Oxidative stress and inflammation were assessed by corresponding kits. M1 macrophage polarization was evaluated via measuring CD86 positive cell rate. The expression levels of ICAM1, ubiquitin\u2010specific peptidase 7 (USP7), and NF\u2010\u03baB pathway\u2010related markers were detected by quantitative real\u2010time PCR and western blot. The interaction between USP7 and ICAM1 was analyzed by Co\u2010IP assay.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>LPS induced apoptosis, inflammation, oxidative stress, and M1 macrophage polarization, while suppressed proliferation in HPMECs. ICAM1 was upregulated in pediatric ARDS patients, and its knockdown alleviated HPMEC injury induced by LPS. USP7 positively regulated ICAM1 protein expression through deubiquitination. USP7 overexpression aggravated LPS\u2010induced HPMEC apoptosis, inflammation, oxidative stress, and M1 macrophage polarization. Besides, ICAM1 upregulation could eliminate the inhibitory effect of USP7 knockdown on LPS\u2010induced HPMEC injury. In addition, USP7 activated NF\u2010\u03baB pathway by promoting ICAM1 expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>USP7\u2010mediated ICAM1 upregulation could promote LPS\u2010induced HPMEC injury by activating NF\u2010\u03baB pathway, which provided a new idea for the treatment of pediatric ARDS.<\/jats:p><\/jats:sec>","DOI":"10.1111\/crj.70079","type":"journal-article","created":{"date-parts":[[2025,5,7]],"date-time":"2025-05-07T03:29:04Z","timestamp":1746588544000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["USP7\u2010Mediated ICAM1 Facilitates Lipopolysaccharide\u2010Induced Human Pulmonary Microvascular Endothelial Cell Injury to Accelerate Pediatric Acute Respiratory Distress Syndrome"],"prefix":"10.1111","volume":"19","author":[{"given":"Jing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Neonatology Chongqing Bishan District Maternal 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