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LncRNA\n                    <jats:italic>GAS5<\/jats:italic>\n                    is closely related to sepsis; however, its detailed functions and mechanism in sepsis\u2010triggered intestinal barrier dysfunction are unclear. In this study, NCM460 cells were stimulated with lipopolysaccharide (LPS) to mimic septic intestinal injury\n                    <jats:italic>in vitro<\/jats:italic>\n                    , and a sepsis mouse model was established via the cecum ligation and perforation method. Terminal deoxynucleotidyl transferase\n                    <jats:styled-content style=\"fixed-case\">dUTP<\/jats:styled-content>\n                    nick end labeling staining was performed for cell apoptosis evaluation. RNA and protein levels were examined by RT\u2010qPCR and western blotting, respectively. Additionally, cell permeability and intestinal mucosa permeability were measured. ELISA was utilized to detect inflammatory cytokine production. H&amp;E staining was conducted for histologic examination of the intestine. Luciferase reporter and RNA pull\u2010down assays were employed to verify the interaction between\n                    <jats:italic>GAS5<\/jats:italic>\n                    ,\n                    <jats:italic>miR\u2010223\u20103p<\/jats:italic>\n                    , and\n                    <jats:italic>FBXW7<\/jats:italic>\n                    . The results showed that\n                    <jats:italic>GAS5<\/jats:italic>\n                    was downregulated in LPS\u2010exposed NCM460 cells as well as the intestine of septic mice.\n                    <jats:italic>GAS5<\/jats:italic>\n                    overexpression mitigated LPS\u2010triggered intestinal epithelial cell damage and apoptosis\n                    <jats:italic>in vitro<\/jats:italic>\n                    and reduced pathological damage, inflammation, and intestinal hyperpermeability in septic mice.\n                    <jats:italic>GAS5<\/jats:italic>\n                    upregulated\n                    <jats:italic>FBXW7<\/jats:italic>\n                    by interacting with\n                    <jats:italic>miR\u2010223\u20103p<\/jats:italic>\n                    . Depletion of\n                    <jats:italic>FBXW7<\/jats:italic>\n                    reversed the protective effects of\n                    <jats:italic>GAS5<\/jats:italic>\n                    overexpression\n                    <jats:italic>in vitro<\/jats:italic>\n                    . Additionally,\n                    <jats:italic>GAS5<\/jats:italic>\n                    overexpression inactivated NF\u2010\u03baB signaling in LPS\u2010stimulated NCM460 cells. NF\u2010\u03baB inactivation exerted effects in septic mice similar to those observed with\n                    <jats:italic>GAS5<\/jats:italic>\n                    overexpression. In conclusion,\n                    <jats:italic>GAS5<\/jats:italic>\n                    ameliorates sepsis\u2010triggered intestinal barrier disruption by mediating the\n                    <jats:italic>miR\u2010223\u20103p<\/jats:italic>\n                    \/\n                    <jats:italic>FBXW7<\/jats:italic>\n                    axis and inactivating NF\u2010\u03baB signaling. \u00a9 2025 The Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.6440","type":"journal-article","created":{"date-parts":[[2025,7,28]],"date-time":"2025-07-28T10:35:15Z","timestamp":1753698915000},"page":"25-39","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["<scp>\n                      LncRNA\n                      <i>GAS5<\/i>\n                    <\/scp>\n                    ameliorates intestinal barrier injury by targeting the\n                    <i>\n                      <scp>miR<\/scp>\n                      \u2010223\u20103p\/\n                      <scp>FBXW7<\/scp>\n                    <\/i>\n                    axis and inactivating\n                    <scp>NF<\/scp>\n                    \u2010\n                    <scp>\u03baB<\/scp>\n                    signaling\n                    <i>in vitro<\/i>\n                    and\n                    <i>in vivo<\/i>"],"prefix":"10.1002","volume":"267","author":[{"given":"Zhen","family":"Wang","sequence":"first","affiliation":[{"name":"Department of General Practice, Yijishan Hospital First Affiliated Hospital of Wannan Medical College  Wuhu PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jin","family":"Yuan","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Yijishan Hospital First Affiliated Hospital of Wannan Medical College  Wuhu PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuemei","family":"Qin","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Yijishan Hospital First Affiliated Hospital of Wannan Medical College  Wuhu PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongzhen","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Yijishan Hospital First Affiliated Hospital of Wannan 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