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However, the regulatory role of lncRNAs in TBI\u2010induced ferroptosis remains poorly understood. This study aims to investigate the role of a specific lncRNA, noncoding transcript of chemokine (C\u2010C motif) ligand 4 (\n                      <jats:italic>Ccl4<\/jats:italic>\n                      ) overlapping (\n                      <jats:italic>Ntoco<\/jats:italic>\n                      ), in the regulation of ferroptosis following TBI and explore its potential as a therapeutic target.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The expression levels of\n                      <jats:italic>Ntoco<\/jats:italic>\n                      following controlled cortical injury (CCI) in mice were measured using real\u2010time PCR. Behavioral tests post\u2010injury were assessed using the rotarod test and Morris water maze, and lesion volume was evaluated using micro\u2010MRI.\n                      <jats:italic>Ntoco<\/jats:italic>\n                      binding proteins were identified using RNA pull\u2010down and RNA immunoprecipitation. RNA sequencing was employed to identify\n                      <jats:italic>Ntoco<\/jats:italic>\n                      \u2010related pathways. Western blotting and co\u2010immunoprecipitation were used to measure protein levels and ubiquitination processes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Ntoco<\/jats:italic>\n                      upregulation was observed in CCI mice.\n                      <jats:italic>Ntoco<\/jats:italic>\n                      knockdown inhibited neuron ferroptosis, reduced lesion volume, and improved spatial memory following TBI.\n                      <jats:italic>Ntoco<\/jats:italic>\n                      overexpression promoted ferroptosis in neurons. Mechanistically,\n                      <jats:italic>Ntoco<\/jats:italic>\n                      facilitated K48\u2010linked ubiquitination and degradation of proteins by binding to Hnrnpab, suppressing the NF\u2010\u03baB\/Lcn2 signaling pathway. This included reduced phosphorylation of IkB\u03b1, increased phosphorylation of IKK\u03b1\/\u03b2, nuclear translocation of the NF\u2010\u03baB p65 subunit, and elevated Lcn2 expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our findings suggest that\n                      <jats:italic>Ntoco<\/jats:italic>\n                      plays a crucial role in TBI\u2010induced ferroptosis by modulating the NF\u2010\u03baB\/Lcn2 signaling pathway. Targeting\n                      <jats:italic>Ntoco<\/jats:italic>\n                      may provide a promising therapeutic strategy to mitigate ferroptosis and improve outcomes following TBI.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/cns.70282","type":"journal-article","created":{"date-parts":[[2025,2,20]],"date-time":"2025-02-20T07:10:57Z","timestamp":1740035457000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["<i>Ntoco<\/i>\n                    Promotes Ferroptosis via Hnrnpab\u2010Mediated\n                    <scp>NF<\/scp>\n                    \u2010\n                    <scp>\u03baB<\/scp>\n                    \/Lcn2 Axis Following Traumatic Brain Injury in Mice"],"prefix":"10.1111","volume":"31","author":[{"given":"Qiang","family":"Wang","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, West China Second University Hospital Sichuan University  Chengdu Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanjun","family":"Zuo","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Histology &amp; Embryology, Faculty of Basic Medical Sciences Kunming Medical University  Kunming Yunnan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huaqin","family":"Sun","sequence":"additional","affiliation":[{"name":"SCU\u2010CUHK Joint Laboratory for Reproductive Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Department of Pediatrics West China Second University Hospital, Sichuan University  Chengdu 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