中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (11): 2383-2384.doi: 10.4103/1673-5374.371354

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

TRPM2和突触外NMDARs功能耦合加剧了缺血性脑损伤的兴奋性毒性

  

  • 出版日期:2023-11-15 发布日期:2023-05-04

Targeting TRPM2- and TRPM4-extrasynaptic N-methyl-D-aspartate receptor coupling in ischemic stroke

Pengyu Zong, Cindy X. Li, Jianlin Feng, Lixia Yue*   

  1. Department of Cell Biology, Calhoun Cardiology Center, UConn Health, Farmington, CT, USA
  • Online:2023-11-15 Published:2023-05-04
  • Contact: Lixia Yue, PhD,lyue@uchc.edu.
  • Supported by:
    We thank the professional proofreading and editing by grant science writers Dr. Christopher Bonin and Dr. Geneva Hargis at UConn Health. 
    We apologize to many peers and colleagues whose elegant work is not cited due to space limitations.
    This work was partially supported by the National Institute of Health (R01-HL143750) and American Heart Association (19TPA34890022) to LY. 

摘要: https://orcid.org/0000-0002-3558-091X (Lixia Yue) 

Abstract: Ischemic stroke represents a heavy burden on public health. Currently, recanalization is the only effective therapy for ischemic stroke in a small population of eligible patients. However, there is no effective adjunct medication for preventing neuron loss after reperfusion to mitigate long-lasting brain injury. Extrasynaptic N-methyl-D-aspartate receptors (esNMDARs) are the major cause of ischemic neuronal death. However, there is no inhibitor selectively targeting esNMDARs without compromising the function of other “beneficial” synaptic NMDARs, which is due to the limited understanding of the underlying molecular mechanisms. Recently, two members of the transient receptor potential melastatin (TRPM) channel family, TRPM2 and TRPM4, were shown to be critical in amplifying esNMDAR-mediated neurotoxic effects during ischemic stroke without influencing the functions of synaptic NMDAR. Targeting the interaction between TRPM2- and TRPM4-esNMDAR provides a novel strategy in screening effective drugs for ischemic stroke.