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The Role of Inflammatory Response in Stroke Associated Programmed Cell Death
K Duris1,2, Z Splichal1, M Jurajda1
1Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Current Neuropharmacology
|February 24, 2018
Summary
Stroke causes primary and secondary brain injury, with the immune system exacerbating damage. This review explores the immune system's role in programmed cell death after stroke and discusses anti-inflammatory therapies.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Stroke is a major cause of death and disability.
- Primary stroke injury involves necrosis from oxygen/glucose deprivation.
- Secondary stroke injury involves apoptosis and potential malignant transformation, often exacerbated by immune responses.
Purpose of the Study:
- To review the immune system's role in stroke pathophysiology.
- To examine the immune system's involvement in programmed neuronal cell death post-stroke.
- To discuss current therapeutic strategies targeting post-stroke inflammation.
Main Methods:
- Literature review of studies on stroke, immune system, and programmed cell death.
- Analysis of the mechanisms linking immune deregulation to secondary brain injury.
- Synthesis of information on therapeutic interventions targeting neuroinflammation.
Main Results:
- The immune system plays a critical role in both initiating and modulating secondary brain injury after stroke.
- Immune cells and mediators contribute significantly to programmed neuronal cell death pathways.
- Dysregulation of the immune system can worsen stroke outcomes.
Conclusions:
- Understanding the immune system's complex role in stroke is crucial for developing effective treatments.
- Targeting neuroinflammation presents a promising therapeutic avenue for mitigating secondary brain injury.
- Further research is needed to optimize immunomodulatory strategies for stroke patients.
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