中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (9): 2004-2009.doi: 10.4103/1673-5374.391181

• 综述:退行性病与再生 • 上一篇    下一篇

半乳糖凝集素 3 在神经炎症和神经退变中的新作用

  

  • 出版日期:2024-09-15 发布日期:2024-01-25

Emerging role of galectin 3 in neuroinflammation and neurodegeneration

Brian M. Lozinski1, #, Khanh Ta2, #, Yifei Dong2, *   

  1. 1Department of Clinical Neuroscience, University of Calgary, Calgary, AB, Canada; 2Deparment of Biochemistry, Microbiology & Immunology, University of Saskatchewan, Saskatoon, SK, Canada
  • Online:2024-09-15 Published:2024-01-25
  • Contact: Yifei Dong, PhD, Jeff.dong@usask.ca.
  • Supported by:
    This work was supported by operating grants from the University of Saskatchewan College of Medicine (to YD), the Natural Sciences and Engineering Research Council of Canada (to YD), MS Canada (to YD), Saskatchewan Health Research Foundation (to YD), and Brain Canada Foundation (to YD) and Doctoral Studentship Support for MS Canada (to BML).

摘要: https://orcid.org/0000-0003-1483-2046 (Yifei Dong)

Abstract: Neuroinflammation and neurodegeneration are key processes that mediate the development and progression of neurological diseases. However, the mechanisms modulating these processes in different diseases remain incompletely understood. Advances in single cell based multi-omic analyses have helped to identify distinct molecular signatures such as Lgals3 that is associated with neuroinflammation and neurodegeneration in the central nervous system (CNS). Lgals3 encodes galectin-3 (Gal3), a β-galactoside and glycan binding glycoprotein that is frequently upregulated by reactive microglia/macrophages in the CNS during various neurological diseases. While Gal3 has previously been associated with non-CNS inflammatory and fibrotic diseases, recent studies highlight Gal3 as a prominent regulator of inflammation and neuroaxonal damage in the CNS during diseases such as multiple sclerosis, Alzheimer’s disease, and Parkinson’s disease. In this review, we summarize the pleiotropic functions of Gal3 and discuss evidence that demonstrates its detrimental role in neuroinflammation and neurodegeneration during different neurological diseases. We also consider the challenges of translating preclinical observations into targeting Gal3 in the human CNS. 

Key words: Alzheimer’s disease, Galectin 3, microglia, multiple sclerosis, neurodegeneration, neuroinflammation, Parkinson’s disease, therapeutics