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Inflammation in the pathogenesis of ischemic stroke
Jian Pei1, Xiaoxin You1, Qinghui Fu1
1Department of Acupuncture, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Frontiers in Bioscience (Landmark Edition)
|January 2, 2015
Summary
Inflammation significantly impacts ischemic stroke, involving complex interactions between pro-inflammatory and anti-inflammatory mediators and immune cells. Understanding these mechanisms is key for developing new stroke treatments.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Ischemic stroke is a leading cause of adult disability globally.
- Inflammation is a critical and complex factor in ischemic stroke pathogenesis.
- An imbalance in pro- and anti-inflammatory mediators drives stroke-related inflammation.
Purpose of the Study:
- To review the roles of inflammatory mediators and immune cells in ischemic stroke.
- To elucidate the complex inflammatory mechanisms underlying ischemic stroke.
- To identify potential therapeutic targets for stroke prevention and treatment.
Main Methods:
- This review synthesizes current research on inflammation in ischemic stroke.
- It examines the involvement of both innate and adaptive immune cells.
- The role of specific mediators like interleukin-17A (IL-17A) is discussed.
Main Results:
- Both pro-inflammatory and anti-inflammatory processes are integral to ischemic stroke.
- Immune cells, including T regulatory cells (Tregs), exhibit dual roles in stroke injury.
- The precise inflammatory cascade in ischemic stroke requires further elucidation.
Conclusions:
- Inflammation is a central component of ischemic stroke pathogenesis.
- Further research into inflammatory mechanisms may yield novel therapeutic strategies.
- Targeting specific inflammatory pathways could improve stroke outcomes.
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