Physiological and Pathophysiological Roles of Transient Receptor Potential Channels in Microglia-Related CNS Inflammatory Diseases

被引:7
|
作者
Shirakawa, Hisashi [1 ]
Kaneko, Shuji [1 ]
机构
[1] Kyoto Univ, Grad Sch Pharmaceut Sci, Dept Mol Pharmacol, Sakyo Ku, 46-29 Yoshida Shimoadachi Cho, Kyoto 6068501, Japan
关键词
microglia; cytokine; transient receptor potential (TRP) channel; central nervous system (CNS) inflammation; Ca2+ signaling; reactive oxygen species; CELL-DEATH; INTRACEREBRAL HEMORRHAGE; TRPM2; CONTRIBUTES; NEUROPATHIC PAIN; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; UP-REGULATION; ION CHANNELS; CA2+ INFLUX; RAT-BRAIN;
D O I
10.1248/bpb.b18-00319
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Central nervous system (CNS) inflammation is a potential therapeutic target for neurodegenerative diseases. In recent years, a number of studies have focused on the links between neurodegenerative diseases and CNS glial cells, especially microglia. Microglia are the main resident immune cells in the CNS and represent approximately 10-15% of all CNS cells. Microglia play an important role in maintaining brain homeostasis at rest by surveying the environment, and engulfing apoptotic cells and debris in the healthy brain. However, under certain pathological conditions, microglia can generate neurotoxic factors, such as pro -inflammatory cytokines and molecules like nitric oxide (NO), which lead to CNS inflammatory diseases. In this review, we discuss the evidence that regulation of microglial ion channels may modulate CNS inflammation and subsequent tissue damage in neurological disorders. In particular, we discuss the role of transient receptor potential (TRP) channels in microglia in both acute and chronic inflammatory conditions, and describe the physiological and pathophysiological roles of TRP channels in CNS inflammatory pathways. Additionally, we describe the benefits of stimulation/inhibition of TRP channels in animal models of microglia-related CNS inflammatory diseases.
引用
收藏
页码:1152 / 1157
页数:6
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