Mechanism of HDAC1 Regulating Iron Overload-Induced Neuronal Oxidative Damage After Cerebral Hemorrhage.
Autor: | Han J; Department of Neurology, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China., Zhang J; Department of Neurology, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China., Yao X; Department of Neurology, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China., Meng M; Department of Neurology, Tianjin Medical University General Hospital Airport Hospital, Tianjin, 300000, China., Wan Y; Department of Neurology, Tianjin Medical University General Hospital Airport Hospital, Tianjin, 300000, China., Cheng Y; Department of Neurology, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China. cchengyan07@163.com. |
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Jazyk: | angličtina |
Zdroj: | Molecular neurobiology [Mol Neurobiol] 2024 Oct; Vol. 61 (10), pp. 7549-7566. Date of Electronic Publication: 2024 Feb 26. |
DOI: | 10.1007/s12035-024-04000-2 |
Abstrakt: | Iron overload is associated with brain edema in the context of intracerebral hemorrhage (ICH). Here, we investigated the role of histone deacetylase 1 (HDAC1) in mediating oxidative damage induced by iron overload after ICH. Utilizing ICH mouse models and FeCl (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.) |
Databáze: | MEDLINE |
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