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Título: | Targeting NRF2 to suppress ferroptosis in brain injury |
Fecha de publicación: | 2021 |
Editorial: | Universidad de Murcia, Departamento de Biologia Celular e Histiologia |
Cita bibliográfica: | Histology and Histopathology Vol. 36, nº4 (2021) |
ISSN: | 0213-3911 1699-5848 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Nuclear Factor Erythroid Related Factor (NRF2) Brain Injury Ferroptosis (FPT) |
Resumen: | y. Brain injury is accompanied by serious iron metabolism disorder and oxidative stress. As a novel form of regulated cell death (RCD) depending on lipid peroxidation caused by iron overload, ferroptosis (FPT) further aggravates brain injury, which is different from apoptosis, autophagy and other traditional cell death in terms of biochemistry, morphology and genetics. Noteworthy, transcriptional regulator NRF2 plays a key role in the cell antioxidant system, and many genes related to FPT are under the control of NRF2, including genes for iron regulation, thiol-dependent antioxidant system, enzymatic detoxification of RCS and carbonyls, NADPH regeneration and ROS sources from mitochondria or extra-mitochondria, which place NRF2 in the key position of regulating the ferroptotic death. Importantly, NRF2 can reduce iron load and resist FPT. In the future, it is expected to open up a new way to treat brain injury by targeting NRF2 to alleviate FPT in brain. |
Autor/es principal/es: | Song, Shunchen Gao, Yaxuan Sheng, Yi Rui, Tongyu Luo, Chengliang |
URI: | http://hdl.handle.net/10201/127106 |
DOI: | https://doi.org/10.14670/HH-18-286 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 15 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
Aparece en las colecciones: | Vol.36, nº4 (2021) |
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Song-36-383-397-2021.pdf | 4,66 MB | Adobe PDF | Visualizar/Abrir |
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