The role of microglial activation on ischemic stroke: Modulation by fibroblast growth factors

Area of Science:

• Neuroscience
• Immunology
• Pharmacology

Background:

• Stroke is a leading cause of death and disability, characterized by reduced oxygen and glucose supply to the brain, triggering inflammation, oxidative stress, and apoptosis.
• Microglia, the central nervous system (CNS) immune cells, play a dual role in stroke, potentially exacerbating damage or promoting tissue repair following ischemic insult.

Purpose of the Study:

• To review current evidence on microglial activation in experimental stroke models.
• To elucidate the pharmacological actions of fibroblast growth factors (FGFs) on microglial modulation.
• To highlight potential therapeutic targets and limitations of FGFs for stroke treatment.

Main Methods:

• Review of existing literature on microglial activation in experimental stroke models.
• Analysis of the role of fibroblast growth factors (FGFs) in regulating microglial responses.
• Examination of the molecular mechanisms underlying FGFs' effects on microglia.

Main Results:

• Microglia activation can either worsen or improve outcomes in experimental stroke models.
• FGFs act as homeostatic factors, influencing metabolism and regulating pro-inflammatory (M1) and anti-inflammatory (M2) cytokine secretion post-stroke.
• FGFs demonstrate pharmacological actions on multiple targets, modulating microglial activity.

Conclusions:

• FGFs offer a potential therapeutic strategy for stroke by targeting microglial modulation.
• Understanding the molecular mechanisms of FGFs is crucial for developing effective stroke treatments.
• Further research is needed to address the limitations and optimize the use of FGFs in clinical stroke therapy.