Glial cells, mainly including astrocytes (19~40%), microglia (10%), and oligodendrocytes (45~75%), have been implicated in neuroinflammation and immune modulation of cerebrovascular diseases. Accumulating evidence suggests glial cells play both beneficial and detrimental roles in cerebrovascular diseases such as stoke and cerebral small-vessel disease (CSVD). Microglia, the resident macrophages in the brain and spinal cord, are the primary mediators of neuroinflammation, exert a dual role in stroke acute phase and recovery stage, which depends on the functional phenotypes of the cells. Astrocyte activation is considered as a key feature of neuroinflammation. Depending on the insults, reactive astrocytes proliferate and release exocytotic gliotransmitters, pro-inflammatory cytokines as well as neurotropic factors. Although the function of glial cells is involved in neuroinflammation, metabolic regulation, angiogenesis, synaptic function and neurogenesis, the underlying mechanisms are still not fully understood.
In this Research Topic, we aim to collect manuscripts including Original Research Articles and Review Papers that elucidate the underlying mechanisms of glial cells participating in pathogenesis of ischemic stroke, hemorrhagic stroke and other cerebrovascular diseases. Meanwhile, we are also interested in research on studying novel therapeutic drug targets and strategies, which improve stroke outcomes and speed up translational application from experimental stroke models to clinical trials.
Therefore, areas of interest include, but are not limited to the following:
• The role of glial cells in stroke and other cerebrovascular diseases.
• Recent advances in basic research in stroke and other cerebrovascular diseases.
• Potential therapeutic drug targets or strategies in stroke and other cerebrovascular diseases.
• Acute phase treatment and long-term recovery after stroke.
• Glial -neuronal interactions after stroke and other cerebrovascular diseases.
Glial cells, mainly including astrocytes (19~40%), microglia (10%), and oligodendrocytes (45~75%), have been implicated in neuroinflammation and immune modulation of cerebrovascular diseases. Accumulating evidence suggests glial cells play both beneficial and detrimental roles in cerebrovascular diseases such as stoke and cerebral small-vessel disease (CSVD). Microglia, the resident macrophages in the brain and spinal cord, are the primary mediators of neuroinflammation, exert a dual role in stroke acute phase and recovery stage, which depends on the functional phenotypes of the cells. Astrocyte activation is considered as a key feature of neuroinflammation. Depending on the insults, reactive astrocytes proliferate and release exocytotic gliotransmitters, pro-inflammatory cytokines as well as neurotropic factors. Although the function of glial cells is involved in neuroinflammation, metabolic regulation, angiogenesis, synaptic function and neurogenesis, the underlying mechanisms are still not fully understood.
In this Research Topic, we aim to collect manuscripts including Original Research Articles and Review Papers that elucidate the underlying mechanisms of glial cells participating in pathogenesis of ischemic stroke, hemorrhagic stroke and other cerebrovascular diseases. Meanwhile, we are also interested in research on studying novel therapeutic drug targets and strategies, which improve stroke outcomes and speed up translational application from experimental stroke models to clinical trials.
Therefore, areas of interest include, but are not limited to the following:
• The role of glial cells in stroke and other cerebrovascular diseases.
• Recent advances in basic research in stroke and other cerebrovascular diseases.
• Potential therapeutic drug targets or strategies in stroke and other cerebrovascular diseases.
• Acute phase treatment and long-term recovery after stroke.
• Glial -neuronal interactions after stroke and other cerebrovascular diseases.
