{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T01:32:46Z","timestamp":1790299966704,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T00:00:00Z","timestamp":1773014400000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82401400"],"award-info":[{"award-number":["82401400"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003819","name":"Natural Science Foundation of Hubei Province","doi-asserted-by":"publisher","award":["2023AFB714"],"award-info":[{"award-number":["2023AFB714"]}],"id":[{"id":"10.13039\/501100003819","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Ferroptosis, an iron\u2010dependent programmed cell death driven by lipid peroxidation, has emerged as a potential contributor to sepsis\u2010associated encephalopathy (SAE). However, the relationship between ferroptosis and cognitive deficits following sepsis needs to be further elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Transcriptome sequencing was employed to identify solute carrier family 40 member 1 (\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      ) as a candidate ferroptosis\u2010related gene in the hippocampus of septic mice. The SAE mouse model was established via cecal ligation and perforation (CLP) after treatment with recombinant adeno\u2010associated virus 9 (AAV9)\u2010CaMKII to knock down or overexpress musculoaponeurotic fibrosarcoma (c\u2010\n                      <jats:italic>Maf<\/jats:italic>\n                      ) or\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      . We assessed cognitive performance, Nissl staining, and ferroptosis\u2010associated parameters. Dual\u2010luciferase reporter gene assays and chromatin immunoprecipitation assays were performed to illuminate the mechanism by which c\u2010MAF transcriptionally activates\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Hippocampal neurons of mice subjected to CLP showed downregulation of\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      . Neuron\u2010specific knockdown of\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      or\n                      <jats:italic>c\u2010Maf<\/jats:italic>\n                      deteriorated sepsis\u2010induced cognitive impairment, oxidative stress, and ferroptosis. Conversely, overexpression of\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      or\n                      <jats:italic>c\u2010Maf<\/jats:italic>\n                      attenuated acute mortality and cognitive impairment following CLP, hampered lipid peroxidation and iron deposition, and enhanced antioxidant capacity. Moreover,\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      silencing neutralized the anti\u2010ferroptotic property of\n                      <jats:italic>c\u2010Maf<\/jats:italic>\n                      in SAE. Mechanistically, c\u2010MAF was found to directly bind to the\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      promoter and facilitate its transcription.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings suggest that c\u2010MAF\/\n                      <jats:italic>Slc40a1<\/jats:italic>\n                      may represent a promising prevention target for SAE.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70820","type":"journal-article","created":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T06:06:38Z","timestamp":1773122798000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["c\u2010\n                    <scp>MAF<\/scp>\n                    Transcriptionally Activates\n                    <i>Slc40a1<\/i>\n                    to Repress Ferroptosis in Sepsis\u2010Associated Encephalopathy"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6944-1558","authenticated-orcid":false,"given":"Wenqin","family":"Song","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Renmin Hospital of Wuhan University  Wuhan Hubei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qianni","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Renmin Hospital of Wuhan University  Wuhan Hubei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9997-4299","authenticated-orcid":false,"given":"Hui","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Perioperative Medicine, Shanghai Key Laboratory of Anesthesiology and Brain Functional Modulation, Clinical Research Center for 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