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Peer-reviewedCC BYGenes & diseases

Glis1 regulates metabolic programming by promoting H3K18 lactylation to alleviate neuronal senescence following spinal cord injury.

  • Dachuan Li1
  • Xiao Lu1
  • Zhaoyang Gong1
  • Jianwei Wu1
  • Yuxuan Zhang1
  • Jiongdong Wu1
  • Chenpei Xu1
  • Xingyu Guo1
  • Guangyu Xu1
  • Haocheng Xu1
  • Shuo Yang1
  • Xinlei Xia1
10 more authors
  • Feizhou Lu1
  • Jianyuan Jiang1
  • Shihao Lu2
  • Junzhe Sheng3
  • Xiaosheng Ma1
  • Wei Zhu1
  • Fei Zou1
  • Chi Sun1
  • Xiaochuan Gu2
  • Yunzhi Guan1
  1. 1Department of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
  2. 2Department of Orthopedics, Changhai Hospital, Navy Medical University, Shanghai 200433, China.
  3. 3Department of Spinal Surgery, Changzheng Hospital, Navy Medical University, Shanghai 200003, China.
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Abstract

Neuronal senescence is a significant factor impeding spinal cord injury (SCI) repair. Research indicates that Glis1, a Kruppel-like zinc finger transcription factor, is pivotal in reprogramming senescent cells and enhancing genomic stability via lactylation. Histone lactylation, an epigenetic modification using lactate as a substrate, becomes prominent post-SCI due to increased neuronal lactate levels. However, the mechanisms linking neuronal senescence and histone lactylation following SCI remain poorly understood. This study elucidates the roles of Glis1, H3K18 lactylation, and neuronal senescence through comprehensive in vivo and in vitro investigations. The findings reveal a post-SCI rise in neuronal lactate levels, accompanied by cellular senescence. Furthermore, upregulation of Glis1 attenuates senescence and promotes histone lactylation. The downstream target secretogranin II (SCG2), identified via ChIP-seq and RNA-seq, was found to exert negative feedback on glycolytic metabolism and lactylation, thereby suppressing neuronal senescence. These results unveil a novel regulatory mechanism of Glis1 in neuronal senescence following SCI through the p300/H3K18la/SCG2 axis, offering a new therapeutic target for spinal cord repair.

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Cite

BibTeXRIS
BibTeX
@article{li2026glis1,
  title = {{Glis1 regulates metabolic programming by promoting H3K18 lactylation to alleviate neuronal senescence following spinal cord injury.}},
  author = {Dachuan Li and Xiao Lu and Zhaoyang Gong and Jianwei Wu and Yuxuan Zhang and Jiongdong Wu and Chenpei Xu and Xingyu Guo and Guangyu Xu and Haocheng Xu and Shuo Yang and Xinlei Xia and Feizhou Lu and Jianyuan Jiang and Shihao Lu and Junzhe Sheng and Xiaosheng Ma and Wei Zhu and Fei Zou and Chi Sun and Xiaochuan Gu and Yunzhi Guan},
  journal = {Genes \& diseases},
  year = {2026},
  month = jul,
  doi = {10.1016/j.gendis.2026.102382},
  url = {https://europepmc.org/article/MED/42898715},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Glis1 regulates metabolic programming by promoting H3K18 lactylation to alleviate neuronal senescence following spinal cord injury.
AU  - Dachuan Li
AU  - Xiao Lu
AU  - Zhaoyang Gong
AU  - Jianwei Wu
AU  - Yuxuan Zhang
AU  - Jiongdong Wu
AU  - Chenpei Xu
AU  - Xingyu Guo
AU  - Guangyu Xu
AU  - Haocheng Xu
AU  - Shuo Yang
AU  - Xinlei Xia
AU  - Feizhou Lu
AU  - Jianyuan Jiang
AU  - Shihao Lu
AU  - Junzhe Sheng
AU  - Xiaosheng Ma
AU  - Wei Zhu
AU  - Fei Zou
AU  - Chi Sun
AU  - Xiaochuan Gu
AU  - Yunzhi Guan
PY  - 2026
DA  - 2026/07/23
JO  - Genes & diseases
DO  - 10.1016/j.gendis.2026.102382
UR  - https://europepmc.org/article/MED/42898715
AB  - Neuronal senescence is a significant factor impeding spinal cord injury (SCI) repair. Research indicates that Glis1, a Kruppel-like zinc finger transcription factor, is pivotal in reprogramming senescent cells and enhancing genomic stability via lactylation. Histone lactylation, an epigenetic modification using lactate as a substrate, becomes prominent post-SCI due to increased neuronal lactate levels. However, the mechanisms linking neuronal senescence and histone lactylation following SCI remain poorly understood. This study elucidates the roles of Glis1, H3K18 lactylation, and neuronal senescence through comprehensive in vivo and in vitro investigations. The findings reveal a post-SCI rise in neuronal lactate levels, accompanied by cellular senescence. Furthermore, upregulation of Glis1 attenuates senescence and promotes histone lactylation. The downstream target secretogranin II (SCG2), identified via ChIP-seq and RNA-seq, was found to exert negative feedback on glycolytic metabolism and lactylation, thereby suppressing neuronal senescence. These results unveil a novel regulatory mechanism of Glis1 in neuronal senescence following SCI through the p300/H3K18la/SCG2 axis, offering a new therapeutic target for spinal cord repair.
SN  - 2352-4820
SN  - 2352-3042
ER  -