Related Experiment Video
Updated: Nov 24, 2025
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
Microglial metabolic disturbances and neuroinflammation in cerebral infarction
Haruna Takeda1, Teruaki Yamaguchi1, Hajime Yano1
1Department of Molecular and Cellular Physiology, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
Abstract:
Cerebral ischemia/reperfusion injury activates microglia, resident immune cells in the brain, and allows the infiltration of circulating immune cells into the ischemic lesions. Microglia play both exacerbating and protective roles in pathological processes and are thus often referred to as "double-edged swords." In ischemic brains, blood-borne macrophages play a role that is distinct from that of resident activated microglia. Recently, the metabolic alteration of immune cells in the pathogenesis of inflammatory disorders including cerebral infarction has become a critical target for investigation. We begin this review by describing the multifaceted functions of microglia in cerebral infarction. Next, we focus on the metabolic alterations that occur in microglia during pathological processes. We also discuss morphological changes that take place in the mitochondria, leading to functional disturbances, accompanied by alterations in microglial function. Moreover, we describe the involvement of the reactive oxygen species that are produced during aberrant metabolic activity. Finally, we discuss therapeutic strategies to ameliorate aggravative changes in metabolism.
Insights
Microglia, crucial brain immune cells, have dual roles in cerebral infarction. Their metabolic changes, mitochondrial dysfunction, and reactive oxygen species production impact stroke outcomes, suggesting new therapeutic targets.
Area of Science:
- Neuroscience
- Immunology
- Metabolism
Background:
- Cerebral ischemia/reperfusion injury activates microglia and recruits peripheral immune cells.
- Microglia exhibit dual roles, both protective and detrimental, in brain injury.
- Metabolic alterations in immune cells are increasingly recognized in cerebral infarction.
Purpose of the Study:
- To review the multifaceted functions of microglia in cerebral infarction.
- To explore metabolic alterations in microglia during pathological processes.
- To discuss therapeutic strategies targeting microglial metabolism.
Main Methods:
- Review of existing literature on microglia, cerebral infarction, and metabolism.
- Analysis of microglial functions, metabolic shifts, and mitochondrial dynamics.
- Examination of reactive oxygen species involvement and potential therapeutic interventions.
Main Results:
- Microglia play complex, context-dependent roles in ischemic stroke.
- Metabolic reprogramming, including mitochondrial dysfunction, significantly impacts microglial activity.
- Aberrant metabolism generates reactive oxygen species, contributing to injury.
Conclusions:
- Microglial metabolism is a critical factor in cerebral infarction pathogenesis.
- Targeting metabolic pathways offers a promising therapeutic avenue for stroke.
- Understanding these mechanisms can lead to novel treatments for brain injury.
