中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (8): 3559-3560.doi: 10.4103/NRR.NRR-D-25-01031

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

Hnrnpu 驱动促星形胶质细胞再生的反应

  

  • 出版日期:2026-08-18 发布日期:2026-04-25

Hnrnpu drives a pro-regenerative astrocyte response

Ruijuan Zhang, Lili Quan, Rieko Muramatsu*   

  1. Department of Molecular Pharmacology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan (Zhang R, Quan L, Muramatsu R)
    Department of NCNP Brain Physiology and Pathology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan (Zhang R)
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Rieko Muramatsu, PhD, muramatsu@ncnp.go.jp.
  • Supported by:
    This work was supported by a Grant-in-Aid of AMED under Grant Numbers (JP22gm1510009) to RM.

摘要: https://orcid.org/0000-0001-5342-7823 (Rieko Muramatsu)

Abstract: Traumatic spinal cord injury (SCI) is a devastating central nervous system (CNS) disorder characterized by significant neurological dysfunction and sensory loss, and effective therapies that prevent neuronal loss and functional recovery remain elusive. After SCI, lesions are surrounded by neuroprotective borders formed by newly proliferated reactive astrocytes. Astrocyte proliferation and activation mediate the formation and function of the glial scar and influence the balance between protection and inflammation. However, molecular mechanisms that regulate these essential astrocytic responses are still poorly understood. Our recent study highlights the DNA/RNA-binding protein, heterogeneous nuclear ribonucleoprotein U (Hnrnpu), as a potential endogenous regulator in astrocyte proliferation, migration, and subsequent scar formation (Quan et al., 2025). Notably, Hnrnpu appears to selectively enhance the expression of permissive extracellular matrix (ECM) molecules, thereby promoting axon regrowth and revealing a pro-regenerative astrocyte response. These findings deepen the understanding of the intrinsic mechanisms that control astrocyte response and provide a new regulatory mechanism involved in reactive astrocyte proliferation and resulting beneficial effects on CNS injury repair. Overall, this work demonstrates the essential function of glial pathology in response to CNS injury and points to a promising therapeutic approach for promoting axon regeneration through targeting astrocytic Hnrnpu to modulate glial scar formation