Molecular and Cellular Mechanisms of Cerebral Ischemia—2nd Edition

Dear Colleagues,

Cerebral ischemia is the leading cause of death worldwide. Despite great efforts to develop potential treatments, the molecular and cellular mechanisms of cerebral ischemia are not yet fully understood.

To date, researchers have employed various animal models of cerebral ischemia with different species of animals, different methods of occlusion of blood vessels, and different periods of occlusion time. Models of cerebral ischemia can be divided into focal and global models. Focal ischemia is characterized by a reduction in cerebral blood flow in a distinct region of the brain. Conversely, in global ischemia, the reduction in blood flow affects the entire brain or forebrain. Neuronal or tissue damage differ according to kind of ischemic injury. In animal models of global transient cerebral or forebrain ischemia, neuronal damage/death (loss) occurs in vulnerable regions of the brain (e.g., hippocampus), whereas in animal models of transient focal bran ischemia, neuronal loss occurs when ischemic duration (damage) is short (mild), or infarction (necrosis) occurs when ischemic damage (duration) is severe (long). In this regard, mechanisms of neuronal loss or infarction vary according to kinds of ischemic insults.

Diverse mechanisms have been suggested for pathophysiological events inflicting ischemic damage, including activation of glutamate receptors, sustained increases in intracellular calcium, oxidative stress caused by free radicals, and the activation of resident microglia related to neuroinflammatory reaction. In addition, the dysfunction of the cells related to the blood–brain barrier (BBB), including endothelial cells, astrocytes and pericytes, as well as microglia, is also suggested as a possible mechanism of ischemic injury.

This Special Issue aims to study the control or modulation of diverse pathways during or after ischemic injuries in molecular and cellular levels in order to prevent, attenuate or heal ischemia damages following various brain ischemic insults.

Prof. Dr. Moo-Ho Won
Guest Editor

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• transient or permanent ischemia
• neuronal death
• necrosis
• inflammation
• oxidative stress
• cytotoxicity
• blood–brain barrier
• neuroprotection
• therapeutic strategy

• Molecular and Cellular Mechanisms of Cerebral Ischemia in Cells (10 articles)