Advances in the research of the role of macrophage/microglia polarization-mediated inflammatory response in spinal cord injury.

Advances in the research of the role of macrophage/microglia polarization-mediated inflammatory response in spinal cord injury.
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巨噬细胞/小胶质细胞极化介导的炎症反应在脊髓损伤中的作用研究进展

DOI:
10.3389/fimmu.2022.1014013
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发表时间:
2022
影响因子:
7.3
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
作者:

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脊髓损伤(spinal cord injury,SCI)后,神经功能的恢复往往是困难的。神经炎症被认为是导致这种失败的原因。调节SCI后的炎症反应可能有助于神经功能的恢复。在过去的几十年里,研究发现巨噬细胞/小胶质细胞是SCI后炎症反应的主要效应细胞之一。越来越多的证据表明,巨噬细胞/小胶质细胞是可塑性细胞,可以响应微环境信号进入M1和M2巨噬细胞/小胶质细胞。M1产生促炎细胞因子以诱导炎症并加重组织损伤,而M2在伤口愈合和组织再生中具有抗炎活性。最近的研究表明,巨噬细胞/小胶质细胞从M1到M2表型的转变支持炎症和组织修复的消退。在这里,我们将回顾炎症反应和巨噬细胞/小胶质细胞在SCI和修复中的作用。此外,我们还将讨论诱导巨噬细胞/小胶质细胞极化的潜在分子机制,重点是调节巨噬细胞/小胶质细胞极化的神经保护疗法,这将为SCI的治疗策略提供新的见解。
It is often difficult to regain neurological function following spinal cord injury (SCI). Neuroinflammation is thought to be responsible for this failure. Regulating the inflammatory response post-SCI may contribute to the recovery of neurological function. Over the past few decades, studies have found that macrophages/microglia are one of the primary effector cells in the inflammatory response following SCI. Growing evidence has documented that macrophages/microglia are plastic cells that can polarize in response to microenvironmental signals into M1 and M2 macrophages/microglia. M1 produces pro-inflammatory cytokines to induce inflammation and worsen tissue damage, while M2 has anti-inflammatory activities in wound healing and tissue regeneration. Recent studies have indicated that the transition from the M1 to the M2 phenotype of macrophage/microglia supports the regression of inflammation and tissue repair. Here, we will review the role of the inflammatory response and macrophages/microglia in SCI and repair. In addition, we will discuss potential molecular mechanisms that induce macrophage/microglia polarization, with emphasis on neuroprotective therapies that modulate macrophage/microglia polarization, which will provide new insights into therapeutic strategies for SCI.
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