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.
Highlights
Stroke is the second leading cause of death worldwide and most victims suffer from disabilities such as paresis and speech defects [1]
We have summarized recent evidence suggesting that microglia have critical functions during ischemic stroke
Inflammation associated with microglia plays an important role in the pathogenesis of ischemic stroke
Summary
Stroke is the second leading cause of death worldwide and most victims suffer from disabilities such as paresis and speech defects [1]. An inflammatory response is initiated within a few hours, with the activation of microglia and astrocytes and the production of chemoattractants, cytokines, and chemokines [6,7,8], with the subsequent infiltration of blood-derived cells such as leukocytes [9, 10]. These cells interact with one another via intricate signaling pathways. We focus on the roles of microglia in neuroinflammation after ischemic stroke
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