Abstract
Ischemic stroke is the main cause of disability worldwide affecting around 6 million deaths per year. A cascade of events following the ischemic insult induce energy failure, excitotoxicity and release of inflammatory mediators that provoke cell death and brain injury. In this process, astrocytes undergo a change on gene expression that leads to reactive astrocytes. In this review, different reactive astrocyte populations have been described, in which A1 neurotoxic astrocytes promote a pro-inflammatory environment and reduce neuronal survival, while A2 neuroprotective astrocytes secrete neurotrophic factors and cytokines that promote tissue repair and axonal regeneration. Therapies based on key targets promoting A2 neuroprotective and reducing A1 phenotypes should be further investigated, as they appear to be promising strategies for a clinically successful stroke therapy.
Keywords
Stroke, Reactive astrocyte, Neuroprotection, Neuroinflammation