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Current Neuropharmacology

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ISSN (Print): 1570-159X
ISSN (Online): 1875-6190

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Review Article

Galectin-3 in Microglia-Mediated Neuroinflammation: Implications for Central Nervous System Diseases

Author(s): Meng-Meng Ge, Nan Chen, Ya-Qun Zhou, Hui Yang, Yu-Ke Tian* and Da-Wei Ye*

Volume 20, Issue 11, 2022

Published on: 20 May, 2022

Page: [2066 - 2080] Pages: 15

DOI: 10.2174/1570159X20666220201094547

Price: $65

Abstract

Microglial activation is one of the common hallmarks shared by various central nervous system (CNS) diseases. Based on surrounding circumstances, activated microglia play either detrimental or neuroprotective effects. Galectin-3 (Gal-3), a group of β-galactoside-binding proteins, has been cumulatively revealed to be a crucial biomarker for microglial activation after injuries or diseases. In consideration of the important role of Gal-3 in the regulation of microglial activation, it might be a potential target for the treatment of CNS diseases. Recently, Gal-3 expression has been extensively investigated in numerous pathological processes as a mediator of neuroinflammation, as well as in cell proliferation. However, the underlying mechanisms of Gal-3 involved in microgliamediated neuroinflammation in various CNS diseases remain to be further investigated. Moreover, several clinical studies support that the levels of Gal-3 are increased in the serum or cerebrospinal fluid of patients with CNS diseases. Thus, we summarized the roles and underlying mechanisms of Gal-3 in activated microglia, thus providing a better insight into its complexity expression pattern, and contrasting functions in CNS diseases.

Keywords: Galectin-3, microglia, neuroinflammation, central nervous system diseases, chronic pain, galectin-3 inhibitor.

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