Regulation of microglial activation in stroke
| Autor: | Fudong Liu, Shou Cai Zhao, Ling Song Ma, Zhao Hu Chu, Wen Qian Wu, Heng Xu |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Ischemia Excitotoxicity Context (language use) Review medicine.disease_cause Neuroprotection Brain Ischemia 03 medical and health sciences 0302 clinical medicine Antigens CD Animals Humans Medicine Pharmacology (medical) Receptors Immunologic Neuroinflammation Inflammation Neurons Pharmacology Microglia business.industry Glutamate receptor Receptor Cross-Talk General Medicine Macrophage Activation medicine.disease Stroke MicroRNAs Oligodendroglia 030104 developmental biology medicine.anatomical_structure nervous system Astrocytes Interferon Regulatory Factors Immunology Tumor necrosis factor alpha Inflammation Mediators business Neuroscience 030217 neurology & neurosurgery Signal Transduction |
| Zdroj: | Acta Pharmacologica Sinica. 38:445-458 |
| ISSN: | 1745-7254 1671-4083 |
| DOI: | 10.1038/aps.2016.162 |
| Popis: | When ischemic stroke occurs, oxygen and energy depletion triggers a cascade of events, including inflammatory responses, glutamate excitotoxicity, oxidative stress, and apoptosis that result in a profound brain injury. The inflammatory response contributes to secondary neuronal damage, which exerts a substantial impact on both acute ischemic injury and the chronic recovery of the brain function. Microglia are the resident immune cells in the brain that constantly monitor brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce both detrimental and neuroprotective mediators, and the balance of the two counteracting mediators determines the fate of injured neurons. The activation of microglia is defined as either classic (M1) or alternative (M2): M1 microglia secrete pro-inflammatory cytokines (TNFα, IL-23, IL-1β, IL-12, etc) and exacerbate neuronal injury, whereas the M2 phenotype promotes anti-inflammatory responses that are reparative. It has important translational value to regulate M1/M2 microglial activation to minimize the detrimental effects and/or maximize the protective role. Here, we discuss various regulators of microglia/macrophage activation and the interaction between microglia and neurons in the context of ischemic stroke. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink