{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T03:03:42Z","timestamp":1778209422269,"version":"3.51.4"},"reference-count":45,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,3,28]],"date-time":"2025-03-28T00:00:00Z","timestamp":1743120000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2025,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Galectin\u20101, a constituent of the mammalian \u03b2\u2010galactoside\u2010binding lectin family, plays a pivotal regulatory role in fibrotic cascades. Dysregulated fibrogenic cellular activity has been implicated as a critical driver of hypertrophic scar (HS) pathogenesis. Nevertheless, the precise mechanistic contributions and molecular pathways through which Galectin\u20101 modulates HS development remain incompletely characterized. qRT\u2010PCR and western blot techniques were employed to explore the expression of Galectin\u20101 in hypertrophic scar tissues and cells. The Galectin\u20101 knockdown cell line was established by utilizing the lentivirus approach, and the influences of Galectin\u20101 on cellular biological functions were examined. The molecular mechanism underlying Galectin\u20101 regulation was investigated via RNA\u2010seq analysis, immunofluorescence, and Western blot. Subsequently, RNA\u2010seq combined with RT\u2010PCR was used to investigate Galectin\u20101's role in HS alternative splicing. Galectin\u20101 exhibits significant overexpression in pathological HS tissues and activated fibroblasts. Genetic silencing of Galectin\u20101 effectively attenuates hypertrophic scar fibroblast (HSF) cell proliferation, migration, and invasive capacities while downregulating fibrotic molecular markers. Transcriptomic and functional analyses reveal that Galectin\u20101 orchestrates concurrent PANoptosis and ferroptosis in fibrogenic cells. Galectin\u20101 regulates PANoptosis through the ROS pathway by modulating the ES alternative splicing of NASP, and this process depends on HNRNPL. Overall, Galectin\u20101 influences the PANoptosis process in HSF cells by modulating the alternative splicing of NASP, thereby regulating the fibrotic cascade. Our findings indicate that Galectin\u20101 is a critical regulator of HS formation, offering a novel therapeutic target and direction for HS treatment.<\/jats:p>","DOI":"10.1096\/fj.202403167r","type":"journal-article","created":{"date-parts":[[2025,3,30]],"date-time":"2025-03-30T16:04:04Z","timestamp":1743350644000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Galectin\u20101 regulates scar hyperplasia by modulating\n                    <scp>NASP<\/scp>\n                    variable splicing to generate\n                    <scp>ROS<\/scp>"],"prefix":"10.1096","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-2604-5390","authenticated-orcid":false,"given":"Yang","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Plastic Surgery The First Affiliated Hospital of Xinjiang Medical University  Urumqi Xinjiang 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