{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T03:10:10Z","timestamp":1791688210731,"version":"4.3.4"},"reference-count":46,"publisher":"Wiley","issue":"19","license":[{"start":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T00:00:00Z","timestamp":1728864000000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82472204"],"award-info":[{"award-number":["82472204"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100012547","name":"Natural Science Foundation of Guangxi Zhuang Autonomous Region","doi-asserted-by":"publisher","award":["GuikeAD22035056"],"award-info":[{"award-number":["GuikeAD22035056"]}],"id":[{"id":"10.13039\/100012547","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Sepsis\u2010associated encephalopathy (SAE) is a serious neurological complication accompanied by acute and long\u2010term cognitive dysfunction. Ferroptosis is a newly discovered type of cell death that is produced by iron\u2010dependent lipid peroxidation. As a key transcriptional coactivator in the Hippo signalling pathway, Yes\u2010associated protein 1 (YAP1) could target ferroptosis\u2010related genes. This study was aimed to determine whether Yap1 protects against SAE and inhibits ferroptosis via maintaining mitochondrial dynamic homeostasis. Caecal ligation puncture (CLP) was used to establish the SAE model, and LPS was applied in hippocampal cells to mimic the inflammatory model in\u00a0vitro. The results showed that Yap1 conditional knockout in hippocampal caused lower survival in SAE mice and cognitive dysfunction, as proved by Morri's water maze (MWM) task, tail suspension test (TST), open field test (OFT) and elevated plus maze test (EPMT). After Yap1 knockout, the production of ROS, MDA and Fe\n                    <jats:sup>2+<\/jats:sup>\n                    and proinflammatory cytokines in the hippocampus were increased, indicating that Yap1 deficiency exacerbates CLP\u2010induced brain injury and hippocampus ferroptosis. Meanwhile, GPX4, SLC7A11, ferritin (FTH1) and GSH levels were decreased in the Yap1 knockout group. In\u00a0vitro, Yap1 overexpression mitigated LPS\u2010induced hippocampal cell ferroptosis and improved mitochondrial function by inhibiting mitochondrial fission, as evidenced by lower mitochondrial ROS, cell viability, Fe\n                    <jats:sup>2+<\/jats:sup>\n                    and the expression of Fis1 and Drp1. Further, the present study suggested that Yap1 could inhibit ferritinophagy\u2010mediated ferroptosis in the hippocampus via inhibiting mitochondrial fission, thus reducing cognitive dysfunction in SAE mice.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.70156","type":"journal-article","created":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T09:50:16Z","timestamp":1728899416000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Yap1 alleviates sepsis associated encephalopathy by inhibiting hippocampus ferroptosis via maintaining mitochondrial dynamic homeostasis"],"prefix":"10.1111","volume":"28","author":[{"given":"Xin","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Zhongnan Hospital of Wuhan University  Wuhan Hubei China"},{"name":"Hubei Provincial Engineering Research Center of Minimally Invasive Cardiovascular Surgery  Wuhan China"},{"name":"Wuhan Clinical 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