{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T19:40:18Z","timestamp":1792611618066,"version":"4.5.0"},"reference-count":30,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T00:00:00Z","timestamp":1775174400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T00:00:00Z","timestamp":1775174400000},"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":["82372207"],"award-info":[{"award-number":["82372207"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82272239"],"award-info":[{"award-number":["82272239"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Magnetic Resonance Imaging"],"published-print":{"date-parts":[[2026,8]]},"abstract":"ABSTRACT<\/jats:title>\n \n Background<\/jats:title>\n The role of ferroptosis in Cardiac arrest (CA)\u2010induced cerebral edema remains unclear.<\/jats:p>\n <\/jats:sec>\n \n Purpose<\/jats:title>\n To investigate whether ferroptosis contributes to blood\u2013brain barrier (BBB) disruption and aquaporin\u20104 (AQP4) dysfunction following CA.<\/jats:p>\n <\/jats:sec>\n \n Study Type<\/jats:title>\n Prospective.<\/jats:p>\n <\/jats:sec>\n \n Animal Model<\/jats:title>\n Asphyxia\u2010induced CA rat model. Forty two rats were used and assigned to the CA (24) and the sham (18) group.<\/jats:p>\n <\/jats:sec>\n \n Field Strength\/Sequence<\/jats:title>\n \n T2\u2010weighted anatomical imaging with 2D turbo spin\u2010echo sequence, QSM with 3D GRE sequence, IVIM with 2D RESOLVE EPI sequence,\n 1<\/jats:sup>\n H\u2010MRS with SVS\u2010PRESS sequence.\n <\/jats:p>\n <\/jats:sec>\n \n Assessment<\/jats:title>\n Multiparametric MRI was performed 24\u2009h after return of spontaneous circulation (ROSC). Imaging findings were validated using histology, immunohistochemistry, Western blot, and transmission electron microscopy.<\/jats:p>\n <\/jats:sec>\n \n Statistical Tests<\/jats:title>\n \n Unpaired two\u2010tailed Student's\n T<\/jats:italic>\n \u2010test was used. A\n p<\/jats:italic>\n value less than 0.05 was considered statistically significant.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n CA led to marked neurological deficits, although no obvious abnormalities were observed on\n T<\/jats:italic>\n 2<\/jats:sub>\n \u2010weighted MRI. QSM revealed marked iron accumulation in the hippocampus, which was associated with elevated ROS, lipid peroxidation, and altered expression of ferroptosis\u2010related markers (downregulation of GPX4 and upregulation of ACSL4). Electron microscopy confirmed mitochondrial changes characteristic of ferroptosis. Ferroptosis\u2010induced lipid peroxidation resulted in degradation of tight\u2010junction proteins (ZO\u20101 and occludin), BBB leakage (elevated serum S100\u03b2), and loss of AQP4 polarity. IVIM showed a selective reduction in true tissue diffusivity (IVIM\n D<\/jats:italic>\n ), indicating cytotoxic edema.\n 1<\/jats:sup>\n H\u2010MRS revealed decreased\n N<\/jats:italic>\n \u2010acetylaspartate, increased lipid peaks, and reduced myo\u2010inositol levels, consistent with neuronal death and astrocytic swelling.\n <\/jats:p>\n <\/jats:sec>\n \n Data Conclusion<\/jats:title>\n This study provides evidence for a sequential cascade after CA and ROSC in which iron overload is associated with ferroptosis, which is linked to disruption of the blood\u2013brain barrier. This barrier disruption coincides with AQP4 depolarization, inducing cytotoxic and vasogenic edema, which, along with depolarization, is accompanied by neuronal death. Multimodal MRI noninvasively captures this process, offering an early detection and monitoring platform for ferroptosis\u2010related brain injury and underscoring its potential as a translational tool for neuroprotective interventions.<\/jats:p>\n <\/jats:sec>\n \n Evidence Level<\/jats:title>\n 1.<\/jats:p>\n <\/jats:sec>\n \n Technical Efficacy<\/jats:title>\n Stage 1.<\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/jmri.70325","type":"journal-article","created":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T04:17:08Z","timestamp":1775276228000},"page":"536-546","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Multimodal\n MR<\/scp>\n Imaging Reveals the Mechanisms of Post\u2010Cardiac\u2010Arrest Brain edema: Ferroptosis\u2010Mediated\n BBB<\/scp>\n Disruption and\n AQP4<\/scp>\n Dysfunction"],"prefix":"10.1002","volume":"64","author":[{"given":"Yunke","family":"Tan","sequence":"first","affiliation":[{"name":"Sun Yat\u2010sen Memorial Hospital, Sun Yat\u2010sen University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"HaoYi","family":"Ye","sequence":"additional","affiliation":[{"name":"The Fourth Affiliated Hospital of Guangzhou Medical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiulin","family":"Ge","sequence":"additional","affiliation":[{"name":"Sun Yat\u2010sen Memorial Hospital, Sun Yat\u2010sen University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3909-3182","authenticated-orcid":false,"given":"Peng","family":"Wang","sequence":"additional","affiliation":[{"name":"Sun Yat\u2010sen Memorial Hospital, Sun Yat\u2010sen University Guangzhou 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