Stroke, including cerebral ischemia, intracerebral hemorrhage, and subarachnoid hemorrhage, is a life-threatening neurological disease characterized by high mortality and morbidity. Oxidative stress is a widespread pathological phenomenon during post-SAH pathological process. Excess reactive oxidative species (ROS) accumulation damages cell components such as DNA, lipids, membranes, and proteins, and leads to neuronal death.

Despite numerous studies focusing on the oxidative stress in neurons, glial cells are also considered as a major target of oxidative stress in the pathological process of stroke. Early views of glia cells as relatively inert, housekeeping cells have evolved, and glia cells are now recognized as dynamic cells that not only respond to neuronal activity but also sense metabolic changes and regulate neuronal metabolism. Accumulating evidence supports the fact that reactive glia cells play important roles in both promoting and limiting brain injury after stroke. In addition, glial activation is also proposed being linked to the pathophysiological process after stroke, such as cellular oxidative stress, apoptosis, endoplasmic reticulum stress and neuroinflammation. Upon activation after stroke, both astrocytes and microglial were showed release radicals, such as superoxide and nitric oxide, that are products of the enzymes NADPH oxidase and inducible nitric oxide synthase. These glial cell - derived radicals, as well as their reactive reaction products hydrogen peroxide and peroxynitrite, have the potential to insult neural cells including glia itself, and have been implicated in contributing to oxidative damage and neuronal cell death in stroke. In contrast, glia cells also contribute efficient antioxidative defense mechanisms for self-protection against oxidative damage after stroke. These cells contain glutathione in high concentrations, substantial activities of the antioxidative enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, as well as NADPH-regenerating enzymes. Their antioxidative potential protects neural cells against oxidative damage. It helps preserve the important functions of these cells in the defense and repair of the brain.

The aim of this Special Issue is to promote research exploring the role of glial cells. Submissions can include astrocytes, oligodendrocytes, NG2-glia, and microglia in oxidative stress after stroke. Research submitted should investigate the pro-oxidative and antioxidative effects after stroke, and underling the molecular mechanism of glia-related ROS circulation. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

• Glial pathology-related oxidative stress after stroke
• Glial-mediated neuronal oxidative stress after stroke
• Relationship between oxidative stress and, astrocytes, and microglial polarization
• Oxidative stress-related subcellular organelle changes in glial cells after stroke
• The molecular mechanisms involved in glia-involved oxidative stress after stroke
• Oxidative stress-related pharmacological targets of glial cells in stroke
• Crosstalk between glial-mediated oxidative stress and other pathological process including programmed cell death, endoplasmic reticulum stress, and neuroinflammation