中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (6): 2345-2346.doi: 10.4103/NRR.NRR-D-25-00550

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

超越神经保护:一氧化碳诱导的少突胶质细胞生成和认知恢复

  

  • 出版日期:2026-06-15 发布日期:2026-04-16

Beyond Neuroprotection: Carbon Monoxide-Induced Oligodendrogenesis and Cognitive Recovery

Shintaro Kimura, Josephine Lok, Ken Arai*   

  1. Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
  • Online:2026-06-15 Published:2026-04-16
  • Contact: Ken Arai, PhD, karai@partners.org.
  • Supported by:
    This work was supported in part by the NIH (R01NS113556, to KA).

摘要: https://orcid.org/0000-0003-1615-3258 (Ken Arai)

Abstract: Carbon monoxide — from toxicity to therapeutic potential: Carbon monoxide (CO) has long been known as a toxic gas, primarily associated with environmental pollution and poisoning. Its strong affinity for hemoglobin causes the formation of carboxyhemoglobin, which reduces oxygen delivery to the tissues and organs and leads to hypoxia. Despite its well-documented toxicity, previous studies have confirmed that CO also acts as a signaling molecule in the body and plays important physiological roles (Motterlini and Otterbein, 2010). This dual nature, both harmful and potentially beneficial, has led to studies of controlled CO exposure in the treatment of central nervous system (CNS) injuries.