KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11

Yi Li; Liangbo Niu; Dai Zheng; Xinxing Zhang; Lu Feng; Jing Fu

doi:10.1038/s42003-024-07251-w

KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11

Commun Biol. 2024 Nov 18;7(1):1530. doi: 10.1038/s42003-024-07251-w.

Authors

Yi Li^#¹, Liangbo Niu^#², Dai Zheng^#¹, Xinxing Zhang³, Lu Feng⁴, Jing Fu⁵

Affiliations

¹ Department of Emergency Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
² Department of Emergency Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
³ Department of Geriatric, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China. [email protected].
⁴ Department of Emergency Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China. [email protected].
⁵ Department of Emergency Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China. [email protected].

^# Contributed equally.

PMID: 39558086
DOI: 10.1038/s42003-024-07251-w

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.