中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (4): 1556-1557.doi: 10.4103/NRR.NRR-D-24-01486

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

腺苷:神经炎症的关键因素

  

  • 出版日期:2026-04-15 发布日期:2025-07-27

Adenosine: A key player in neuroinflammation

Qilin Guo, Rhea Seth, Wenhui Huang*   

  1. Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, Homburg, Germany
  • Online:2026-04-15 Published:2025-07-27
  • Contact: Wenhui Huang, PhD, wenhui.huang@uks.eu.
  • Supported by:
    We thank Dr. Frank Kirchhoff (University of Saarland, Germany) for his generous support to our work in all aspects. This work was supported by grants from the Deutsche Forschungsgemeinschaft (HU 2614/1-1 (Project No. 462650276), the Fritz Thyssen Foundation (10.21.1.021MN) and the Medical faculty of the University of Saarland (HOMFOR2016, HOMFORexzellent2017, HOMFOR2024 Anschubfinanzierung) to WH.

摘要: https://orcid.org/0000-0001-9865-0375 (Wenhui Huang)

Abstract: Neuroinflammation, the inflammatory response of the central nervous system (CNS), is a common feature of many neurological disorders such as sepsis-associated encephalopathy (SAE), multiple sclerosis (MS), and Parkinson’s disease (PD). Prior studies identified cytokines (e.g., tumor necrosis factor [TNF], interleukin [IL]-1, and IL-6) delivered by resident glial cells and brain-invading peripheral immune cells as the major contributor to neuroinflammation (Becher et al., 2017). In addition to pro-inflammatory cytokines, elevated levels of extracellular purine molecules such as adenosine triphosphate (ATP) and adenosine can be detected upon any pathological insults (e.g., injury, ischemia, and hypoxia), contributing to the progression of neurological disorders (Borea et al., 2017).