Skip to main page content
U.S. flag

An official website of the United States government

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Oct 20;27(20):7080.
doi: 10.3390/molecules27207080.

Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage

Yuting Guo  1 , Weibo Dai  2 , Yan Zheng  3 , Weilin Qiao  4 , Weixuan Chen  4 , Lihua Peng  4 , Hua Zhou  5 , Tingting Zhao  6 , Huimin Liu  1 , Feng Zheng  7 , Peng Sun  8
Affiliations
Review

Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage

Yuting Guo et al. Molecules. .

Abstract

Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke, but effective treatments are lacking, and neuroinflammation plays a key role in the pathogenesis. In the innate immune response to cerebral hemorrhage, microglia first appear around the injured tissue and are involved in the inflammatory cascade response. Microglia respond to acute brain injury by being activated and polarized to either a typical M1-like (pro-inflammatory) or an alternative M2-like (anti-inflammatory) phenotype. These two polarization states produce pro-inflammatory or anti-inflammatory. With the discovery of the molecular mechanisms and key signaling molecules related to the polarization of microglia in the brain, some targets that regulate the polarization of microglia to reduce the inflammatory response are considered a treatment for secondary brain tissue after ICH damage effective strategies. Therefore, how to promote the polarization of microglia to the M2 phenotype after ICH has become the focus of attention in recent years. This article reviews the mechanism of action of microglia's M1 and M2 phenotypes in secondary brain injury after ICH. Moreover, it discusses compounds and natural pharmaceutical ingredients that can polarize the M1 to the M2 phenotype.

Keywords: inflammatory response; intracerebral hemorrhage; microglia polarization; therapeutic target.

PubMed Disclaimer

Conflict of interest statement

All authors declare that there are no conflict of interest.

Figures

Figure 1
Figure 1
Mechanism of microglia polarization after cerebral hemorrhage.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Magid-Bernstein J., Girard R., Polster S., Srinath A., Romanos S., Awad I.A., Sansing L.H. Cerebral Hemorrhage: Pathophysiology, Treatment, and Future Directions. Circ. Res. 2022;130:1204–1229. doi: 10.1161/CIRCRESAHA.121.319949. - DOI - PMC - PubMed
    1. Zhu H., Wang Z., Yu J., Yang X., He F., Liu Z., Che F., Chen X., Ren H., Hong M., et al. Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage. Prog. Neurobiol. 2019;178:101610. doi: 10.1016/j.pneurobio.2019.03.003. - DOI - PubMed
    1. Lan X., Han X., Li Q., Yang Q.W., Wang J. Modulators of microglial activation and polarization after intracerebral haemorrhage. Nat. Rev. Neurol. 2017;13:420–433. doi: 10.1038/nrneurol.2017.69. - DOI - PMC - PubMed
    1. Tschoe C., Bushnell C.D., Duncan P.W., Alexander-Miller M.A., Wolfe S.Q. Neuroinflammation after Intracerebral Hemorrhage and Potential Therapeutic Targets. J. Stroke. 2020;22:29–46. doi: 10.5853/jos.2019.02236. - DOI - PMC - PubMed
    1. Fumagalli S., Perego C., Pischiutta F., Zanier E.R., De Simoni M.G. The ischemic environment drives microglia and macrophage function. Front. Neurol. 2015;6:81. doi: 10.3389/fneur.2015.00081. - DOI - PMC - PubMed

MeSH terms

Substances