Microglia-mediated neuroinflammation and neuroplasticity after stroke.

Microglia-mediated neuroinflammation and neuroplasticity after stroke.
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DOI:
10.3389/fncel.2022.980722
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发表时间:
2022
影响因子:
5.3
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
作者:

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中风仍然是全球长期残疾和死亡的主要原因。免疫系统在决定中风后大脑的状况方面起着重要作用。作为中枢神经系统的固有免疫细胞,小胶质细胞是覆盖整个脑实质的防御网络中的主要应答者,并且在生理或病理条件下取决于与神经元、星形胶质细胞和其他邻近细胞的动态通信而发挥各种功能。小胶质细胞的活化和极化对缺血性脑卒中后的脑损伤和修复至关重要,被认为是神经恢复的双刃剑。小胶质细胞可以以促炎状态存在,促进继发性脑损伤,但它们也可以分泌抗炎细胞因子和神经营养因子,促进脑卒中后的恢复。本文就缺血后小胶质细胞介导的神经炎症和神经可塑性的作用和机制以及相关的基于小胶质细胞的干预治疗脑卒中的研究进展作一综述。
Stroke remains a major cause of long-term disability and mortality worldwide. The immune system plays an important role in determining the condition of the brain following stroke. As the resident innate immune cells of the central nervous system, microglia are the primary responders in a defense network covering the entire brain parenchyma, and exert various functions depending on dynamic communications with neurons, astrocytes, and other neighboring cells under both physiological or pathological conditions. Microglia activation and polarization is crucial for brain damage and repair following ischemic stroke, and is considered a double-edged sword for neurological recovery. Microglia can exist in pro-inflammatory states and promote secondary brain damage, but they can also secrete anti-inflammatory cytokines and neurotrophic factors and facilitate recovery following stroke. In this review, we focus on the role and mechanisms of microglia-mediated neuroinflammation and neuroplasticity after ischemia and relevant potential microglia-based interventions for stroke therapy.
干扰素调节因子 4/5 信号传导对小鼠缺血性中风后小胶质细胞活化的影响。
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