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Review
. 2022 Aug 16:16:980722.
doi: 10.3389/fncel.2022.980722. eCollection 2022.

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Yuan Wang  1 , Rehana K Leak  2 , Guodong Cao  1   3
Affiliations
Review

Microglia-mediated neuroinflammation and neuroplasticity after stroke

Yuan Wang et al. Front Cell Neurosci. .

Abstract

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.

Keywords: brain repair; ischemic stroke; microglia; neuroinflammation; plasticity.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Microglia crosstalk with other cells in the brain post ischemic injury.
See this image and copyright information in PMC

References

    1. Aboutaleb N., Faezi M., Nasseri Maleki S., Nazarinia D., Razavi Tousi S. M. T., Hashemirad N., et al. . (2019). Conditioned medium obtained from mesenchymal stem cells attenuates focal cerebral ischemia reperfusion injury through activation of ERK1/ERK2-BDNF signaling pathway. J. Chem. Neuroanat. 97, 87–98. 10.1016/j.jchemneu.2019.02.003 - DOI - PubMed
    1. Abumaree M., Al Jumah M., Pace R. A., Kalionis B. (2012). Immunosuppressive properties of mesenchymal stem cells. Stem Cell Rev. Rep. 8, 375–392. 10.1007/s12015-011-9312-0 - DOI - PubMed
    1. Ahmed S. M., Luo L., Namani A., Wang X. J., Tang X. (2017). Nrf2 signaling pathway: pivotal roles in inflammation. Biochim. Biophys. Acta. Mol. Basis. Dis. 1863, 585–597. 10.1016/j.bbadis.2016.11.005 - DOI - PubMed
    1. Ahn J. H., Kim D. W., Park J. H., Lee T. K., Lee H. A., Won M. H., et al. . (2019). Expression changes of CX3CL1 and CX3CR1 proteins in the hippocampal CA1 field of the gerbil following transient global cerebral ischemia. Int. J. Mol. Med. 44, 939–948. 10.3892/ijmm.2019.4273 - DOI - PMC - PubMed
    1. Al Mamun A., Chauhan A., Qi S., Ngwa C., Xu Y., Sharmeen R., et al. . (2020). Microglial IRF5-IRF4 regulatory axis regulates neuroinflammation after cerebral ischemia and impacts stroke outcomes. Proc. Natl. Acad. Sci. U S A 117, 1742–1752. 10.1073/pnas.1914742117 - DOI - PMC - PubMed