Microglial metabolic disturbances and neuroinflammation in cerebral infarction

被引:181
|
作者
Takeda, Haruna [1 ]
Yamaguchi, Teruaki [1 ]
Yano, Hajime [1 ]
Tanaka, Junya [1 ]
机构
[1] Ehime Univ, Grad Sch Med, Dept Mol & Cellular Physiol, Toon, Ehime 7910295, Japan
基金
日本学术振兴会;
关键词
ROS; Glycolysis; OXPHOS; Macrophage; Nrf2; ISCHEMIC-STROKE; RAT-BRAIN; POSTISCHEMIC INFLAMMATION; ACTIVATED MICROGLIA; NADPH OXIDASE; CELLS; INJURY; MACROPHAGES; NRF2; MITOCHONDRIA;
D O I
10.1016/j.jphs.2020.11.007
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cerebral ischemia/reperfusion injury activates microglia, resident immune cells in the brain, and allows the infiltration of circulating immune cells into the ischemic lesions. Microglia play both exacerbating and protective roles in pathological processes and are thus often referred to as "double-edged swords." In ischemic brains, blood-borne macrophages play a role that is distinct from that of resident activated microglia. Recently, the metabolic alteration of immune cells in the pathogenesis of inflammatory disorders including cerebral infarction has become a critical target for investigation. We begin this review by describing the multifaceted functions of microglia in cerebral infarction. Next, we focus on the metabolic alterations that occur in microglia during pathological processes. We also discuss morphological changes that take place in the mitochondria, leading to functional disturbances, accompanied by alterations in microglial function. Moreover, we describe the involvement of the reactive oxygen species that are produced during aberrant metabolic activity. Finally, we discuss therapeutic strategies to ameliorate aggravative changes in metabolism. (C) 2020 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.
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页码:130 / 139
页数:10
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