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Biomed Res Int. 2014;2014:297241. doi: 10.1155/2014/297241. Epub 2014 Jun 25.

Therapeutically targeting neuroinflammation and microglia after acute ischemic stroke.

Author information

1
National Primate Research Center (NPRC), Korea Research Institute of Bioscience and Biotechnology (KRIBB), Ochang 363-883, Republic of Korea.
2
Medical Research Institute, Chung-Ang University College of Medicine, Seoul 156-756, Republic of Korea.

Abstract

Inflammation has a pivotal role in the pathogenesis of ischemic stroke, and recent studies posit that inflammation acts as a double-edged sword, not only detrimentally augmenting secondary injury, but also potentially promoting recovery. An initial event of inflammation in ischemic stroke is the activation of microglia, leading to production of both pro- and anti-inflammatory mediators acting through multiple receptor signaling pathways. In this review, we discuss the role of microglial mediators in acute ischemic stroke and elaborate on preclinical and clinical studies focused on microglia in stroke models. Understanding how microglia can lead to both pro- and anti-inflammatory responses may be essential to implement therapeutic strategies using immunomodulatory interventions in ischemic stroke.

PMID:
25089266
PMCID:
PMC4095830
DOI:
10.1155/2014/297241
[Indexed for MEDLINE]
Free PMC Article

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