Yi Li, Liangbo Niu, Dai Zheng, Xinxing Zhang, Lu Feng, Jing Fu
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KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11.
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.
期刊介绍：
Communications Biology is an open access journal from Nature Research publishing high-quality research, reviews and commentary in all areas of the biological sciences. Research papers published by the journal represent significant advances bringing new biological insight to a specialized area of research.
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