KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11
Abstract Ischemic stroke poses a significant global health risk. Currently, recanalization of blood flow through surgery or medication is the only effective means to control ischemia-reperfusion injury. This study aims to explore the role and molecular mechanism of OGT in regulating neuronal injury...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2024-11-01
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| Series: | Communications Biology |
| Online Access: | https://doi.org/10.1038/s42003-024-07251-w |
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| author | Yi Li Liangbo Niu Dai Zheng Xinxing Zhang Lu Feng Jing Fu |
| author_facet | Yi Li Liangbo Niu Dai Zheng Xinxing Zhang Lu Feng Jing Fu |
| author_sort | Yi Li |
| collection | DOAJ |
| description | Abstract Ischemic stroke poses a significant global health risk. Currently, recanalization of blood flow through surgery or medication is the only effective means to control ischemia-reperfusion injury. This study aims to explore the role and molecular mechanism of OGT in regulating neuronal injury and motor deficits following a stroke. The MCAO and OGD/R models were established to validate the therapeutic efficacy of OGT in mitigating neuronal injury and motor dysfunction following stroke. Molecular biological techniques were employed to assess ferroptosis levels, OGT ubiquitination, and SLC7A11 O-GlcNAcylation. OGT has a therapeutic effect on motor deficits and neuronal damage after stroke by regulating SLC7A11 O-GlcNacylation-mediated ferroptosis, while the KDM2B-mediated ubiquitination pathway is responsible for changes in OGT levels. These findings are crucial for target selection and biomarker identification in stroke treatment. |
| format | Article |
| id | doaj-art-e1f2ee6e513c4896af73550270de51d0 |
| institution | OA Journals |
| issn | 2399-3642 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Communications Biology |
| spelling | doaj-art-e1f2ee6e513c4896af73550270de51d02025-08-20T02:22:21ZengNature PortfolioCommunications Biology2399-36422024-11-017111610.1038/s42003-024-07251-wKDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11Yi Li0Liangbo Niu1Dai Zheng2Xinxing Zhang3Lu Feng4Jing Fu5Department of Emergency Medicine, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of ChinaDepartment of Emergency Surgery, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of ChinaDepartment of Emergency Medicine, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of ChinaDepartment of Geriatric, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of ChinaDepartment of Emergency Surgery, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of ChinaDepartment of Emergency Medicine, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of ChinaAbstract Ischemic stroke poses a significant global health risk. Currently, recanalization of blood flow through surgery or medication is the only effective means to control ischemia-reperfusion injury. This study aims to explore the role and molecular mechanism of OGT in regulating neuronal injury and motor deficits following a stroke. The MCAO and OGD/R models were established to validate the therapeutic efficacy of OGT in mitigating neuronal injury and motor dysfunction following stroke. Molecular biological techniques were employed to assess ferroptosis levels, OGT ubiquitination, and SLC7A11 O-GlcNAcylation. OGT has a therapeutic effect on motor deficits and neuronal damage after stroke by regulating SLC7A11 O-GlcNacylation-mediated ferroptosis, while the KDM2B-mediated ubiquitination pathway is responsible for changes in OGT levels. These findings are crucial for target selection and biomarker identification in stroke treatment.https://doi.org/10.1038/s42003-024-07251-w |
| spellingShingle | Yi Li Liangbo Niu Dai Zheng Xinxing Zhang Lu Feng Jing Fu KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11 Communications Biology |
| title | KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11 |
| title_full | KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11 |
| title_fullStr | KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11 |
| title_full_unstemmed | KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11 |
| title_short | KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11 |
| title_sort | kdm2b regulates stroke injury by modulating ogt mediated 0 glcnacylation of slc7a11 |
| url | https://doi.org/10.1038/s42003-024-07251-w |
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