4.7 Review

Treatment targets for M2 microglia polarization in ischemic stroke

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 105, Issue -, Pages 518-525

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.05.143

Keywords

Microglia; M2 polarization; Ischemic stroke; Inflammation; Neuroprotection

Funding

  1. Natural Science Foundation of Jiangsu Province, China [BK20140286]
  2. National Natural Science Foundation of China [81471202]

Ask authors/readers for more resources

As the first line of defense in the nervous system, resident microglia are the predominant immune cells in the brain. In diseases of the central nervous system such as stroke, Alzheimer's disease, and Parkinson's disease, they often cause inflammation or phagocytosis; however, some studies have found that despite the current controversy over M1, M2 polarization could be beneficial. Ischemic stroke is the third most common cause of death in humans. Patients who survive an ischemic stroke might experience a clear decline in their quality of life, owing to conditions such as hemiplegic paralysis and aphasia. After stroke, the activated microglia become a double-edged sword, with distinct phenotypic changes to the deleterious M1 and neuroprotective M2 types. Therefore, methods for promoting the differentiation of microglia into the M2 polarized form to alleviate harmful reactions after stroke have become a topic of interest in recent years. Subsequently, the discovery of new drugs related to M2 polarization has enabled the realization of targeted therapies. In the present review, we discussed the neuroprotective effects of microglia M2 polarization and the potential mechanisms and drugs by which microglia can be transformed into the M2 polarized type after stroke.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available