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Peer-reviewedCC BYBiomaterials research

Glial Scar-Targeted Modification of Hepatocyte Growth Factor-Derived Peptide for Spinal Cord Injury Therapeutic Repair.

  • Yuzhe Wu1,2
  • Jingwei Shi3
  • Ruize Miao1,2
  • Linyi Xiang1,2
  • Jiacheng Zhang1,2
  • Weiyi Chi4
  • Yuheng Zhang5
  • Yibo Geng6
  • Xiong Cai7
  • Yun Shu1,2
  • Jiayi Zhao1,2
  • Junsheng Zhu1,2
9 more authors
  • Xiaoqiong Jiang8
  • Haojie Zhang9
  • Zhenglin Li3,8,10
  • Xiangyang Wang1,2
  • Sunren Sheng1,2
  • Chenchen Zhu11
  • Jianjun Qi12
  • Jian Xiao1,3,8,10
  • Kailiang Zhou1,2,3
12 affiliations
  1. 1Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
  2. 2Zhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou 325027, China.
  3. 3Cixi Biomedical Research Institute, Wenzhou Medical University, Ningbo 315300, China.
  4. 4The First Clinical Medical College (School of Information and Engineering), Wenzhou Medical University, Wenzhou 325035, China.
  5. 5The Second Clinical Medical College of Wenzhou Medical University, Wenzhou 325027, China.
  6. 6Department of Orthopaedics, Tangdu Hospital, The Air Force Medical University, Xi'an 710038, China.
  7. 7School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou 325000, China.
  8. 8Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  9. 9Department of Orthopedics, Xuanwu Hospital of Capital Medical University, Beijing 100053, China.
  10. 10Department of Wound Repair, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
  11. 11Department of Ophthalmology, The First Affiliated Hospital of Bengbu Medical University, Bengbu 233000, China.
  12. 12Department of Laboratory Medicine, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu 241001, China.
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Abstract

Spinal cord injury (SCI) causes irreversible neural damage and functional impairment. H-RN is a short peptide originating from the kringle 1 domain of hepatocyte growth factor. Despite its efficacy in inhibiting inflammatory responses, the precise neuroprotective mechanisms of the peptide H-RN in SCI remain unclear. The short peptide CAQK can target the lesion epicenter of SCI. To explore the role of the peptide H-RN in SCI and address the numerous challenges faced by conventional drug therapies, this study developed a synthetic peptide, CAQK-H-RN. Our results revealed that CAQK-H-RN could cross the blood-spinal cord barrier, precisely target the SCI region, and increase drug accumulation at the injury site, thereby reducing glial scar formation, decreasing motor neuron death, and enhancing functional recovery after SCI. RNA sequencing was performed to explore the molecular mechanisms of CAQK-H-RN in SCI, which revealed that CAQK-H-RN inhibited pyroptosis and ameliorated lysosomal membrane permeabilization (LMP)-induced autophagic flux disorders in neurons after SCI. Additionally, CAQK-H-RN alleviated LMP by suppressing acid sphingomyelinase activity through the p38 mitogen-activated protein kinase/Ets-like protein-1 (Elk-1)/early growth response protein 1 (Egr-1) signaling cascade and subsequently enhanced autophagy, thereby mitigating neuronal death. This intravenous therapeutic system centered on the synthetic peptide CAQK-H-RN contributes to the functional restoration of SCI, which may be clinically applicable to spinal cord repair.

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Cite

BibTeXRIS
BibTeX
@article{wu2026glial,
  title = {{Glial Scar-Targeted Modification of Hepatocyte Growth Factor-Derived Peptide for Spinal Cord Injury Therapeutic Repair.}},
  author = {Yuzhe Wu and Jingwei Shi and Ruize Miao and Linyi Xiang and Jiacheng Zhang and Weiyi Chi and Yuheng Zhang and Yibo Geng and Xiong Cai and Yun Shu and Jiayi Zhao and Junsheng Zhu and Xiaoqiong Jiang and Haojie Zhang and Zhenglin Li and Xiangyang Wang and Sunren Sheng and Chenchen Zhu and Jianjun Qi and Jian Xiao and Kailiang Zhou},
  journal = {Biomaterials research},
  year = {2026},
  month = oct,
  doi = {10.34133/bmr.0431},
  url = {https://europepmc.org/article/MED/42947949},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Glial Scar-Targeted Modification of Hepatocyte Growth Factor-Derived Peptide for Spinal Cord Injury Therapeutic Repair.
AU  - Yuzhe Wu
AU  - Jingwei Shi
AU  - Ruize Miao
AU  - Linyi Xiang
AU  - Jiacheng Zhang
AU  - Weiyi Chi
AU  - Yuheng Zhang
AU  - Yibo Geng
AU  - Xiong Cai
AU  - Yun Shu
AU  - Jiayi Zhao
AU  - Junsheng Zhu
AU  - Xiaoqiong Jiang
AU  - Haojie Zhang
AU  - Zhenglin Li
AU  - Xiangyang Wang
AU  - Sunren Sheng
AU  - Chenchen Zhu
AU  - Jianjun Qi
AU  - Jian Xiao
AU  - Kailiang Zhou
PY  - 2026
DA  - 2026/10/27
JO  - Biomaterials research
DO  - 10.34133/bmr.0431
UR  - https://europepmc.org/article/MED/42947949
AB  - Spinal cord injury (SCI) causes irreversible neural damage and functional impairment. H-RN is a short peptide originating from the kringle 1 domain of hepatocyte growth factor. Despite its efficacy in inhibiting inflammatory responses, the precise neuroprotective mechanisms of the peptide H-RN in SCI remain unclear. The short peptide CAQK can target the lesion epicenter of SCI. To explore the role of the peptide H-RN in SCI and address the numerous challenges faced by conventional drug therapies, this study developed a synthetic peptide, CAQK-H-RN. Our results revealed that CAQK-H-RN could cross the blood-spinal cord barrier, precisely target the SCI region, and increase drug accumulation at the injury site, thereby reducing glial scar formation, decreasing motor neuron death, and enhancing functional recovery after SCI. RNA sequencing was performed to explore the molecular mechanisms of CAQK-H-RN in SCI, which revealed that CAQK-H-RN inhibited pyroptosis and ameliorated lysosomal membrane permeabilization (LMP)-induced autophagic flux disorders in neurons after SCI. Additionally, CAQK-H-RN alleviated LMP by suppressing acid sphingomyelinase activity through the p38 mitogen-activated protein kinase/Ets-like protein-1 (Elk-1)/early growth response protein 1 (Egr-1) signaling cascade and subsequently enhanced autophagy, thereby mitigating neuronal death. This intravenous therapeutic system centered on the synthetic peptide CAQK-H-RN contributes to the functional restoration of SCI, which may be clinically applicable to spinal cord repair.
SN  - 1226-4601
SN  - 2055-7124
ER  -