{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T08:27:58Z","timestamp":1786523278931,"version":"build-2736575974"},"reference-count":46,"publisher":"SAGE Publications","issue":"10-12","license":[{"start":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T00:00:00Z","timestamp":1782691200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"the Nature Science Fundation of Hebei Province","award":["C2025205065"],"award-info":[{"award-number":["C2025205065"]}]},{"name":"the Nature Science Fundation of Hebei Province","award":["H2024206372"],"award-info":[{"award-number":["H2024206372"]}]},{"name":"the Key Project of the Natural Science Foundation of Hebei Province, China","award":["E2021205003"],"award-info":[{"award-number":["E2021205003"]}]},{"name":"Hebei Province Government-funded Excellent Talents Project in Clinical Medicine","award":["ZF2024147"],"award-info":[{"award-number":["ZF2024147"]}]},{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["82301458"],"award-info":[{"award-number":["82301458"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["U23A20169"],"award-info":[{"award-number":["U23A20169"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2026,10,1]]},"abstract":"<jats:sec>\n                    <jats:title>Aim:<\/jats:title>\n                    <jats:p>The activation of microglia triggers an inflammatory response, which is frequently associated with an imbalance of iron metabolism. This study aimed to determine whether inflammation-associated iron dyshomeostasis contributes to impaired poststroke recovery and to explore the underlying mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Ferroportin 1 (FPN1) deficiency in neurons and glial cells delayed sensorimotor function recovery following cerebral ischemia. FPN1 deficiency was associated with aggravated neuronal injury, enhanced apoptosis- and necroptosis-associated signaling, impaired myelin- and synapse-related repair, and reduced dendritic spine density in the ischemic cortex. Histological analyses, including hematoxylin and eosin staining and Nissl staining, further supported more severe peri-infarct pathological damage in\n                      <jats:italic toggle=\"yes\">\n                        Fpn1\n                        <jats:sup>Nestin<\/jats:sup>\n                      <\/jats:italic>\n                      -CKO mice. In addition, increased IgG extravasation indicated aggravated blood\u2013brain barrier (BBB) disruption and secondary neurovascular injury after stroke. These pathological changes were accompanied by increased iron accumulation in the ischemic cortex and altered expression of iron metabolism-related molecules. Elevated inflammatory cytokine expression and increased hepcidin levels were associated with disrupted brain iron homeostasis in\n                      <jats:italic toggle=\"yes\">\n                        Fpn1\n                        <jats:sup>Nestin<\/jats:sup>\n                      <\/jats:italic>\n                      -CKO mice. Inhibition of JAK-STAT signaling with AG490 reduced p-STAT3 and hepcidin levels and was associated with modulation of iron-related and repair-associated responses, with more pronounced effects observed in\n                      <jats:italic toggle=\"yes\">Fpn1<\/jats:italic>\n                      -deficient mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation and Conclusion:<\/jats:title>\n                    <jats:p>\n                      These findings highlight a close association between inflammatory signaling, BBB dysfunction, and iron dyshomeostasis during poststroke recovery. Our results suggest that delayed sensorimotor recovery in mice with neuronal and glial FPN1 deficiency may be linked to inflammation-associated BBB disruption and subsequent iron accumulation in the ischemic brain.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      45, 417\u2013434.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/15230864261464407","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T01:46:01Z","timestamp":1782783961000},"page":"417-434","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Inflammation Impairs Poststroke Recovery by Disrupting Iron Homeostasis in Brain"],"prefix":"10.1177","volume":"45","author":[{"given":"Xin","family":"Guo","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Sciences, Hebei Normal University, Shijiazhuang, China."},{"name":"Department of Neurology, Psychosomatic Medicine Engineering Research Center of Hebei Province, Neuromedical Technology Innovation Center of Hebei Province, The First Hospital of Hebei Medical University, Shijiazhuang, China."},{"name":"Department of Neurology, Hebei Hospital, Xuanwu Hospital, Capital Medical University, Shijiazhuang, China."},{"name":"State Key Laboratory of Neurology and Oncology Drug Development, Nanjing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaofang","family":"Jin","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Sciences, Hebei Normal University, Shijiazhuang, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaomeng","family":"Kang","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, 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