Following brain injuries, the cross-talk between neurons, glia, and vascular elements is greatly disrupted. Emerging experimental investigations suggested vascular failure is one of the key pathogenic factors, which essentially underlies the damaging secondary events, featured in early capillary permeability disruption resulting in producing cerebral edema, inflammation, and secondary neuron death. At delayed phases, vascular remodeling, particularly in angiogenesis and enhanced endothelial-derived trophic factor secretion, may promote endogenous neurogenesis and neuronal repair. Hence, novel therapy targeting early and delayed neurovascular dysfunction might provide promising opportunities to improve clinical outcomes for patients following brain injuries.
Till now, our understanding of neurovascular dysfunction in brain injuries was greatly expanded. Blood-brain barrier disruption is associated with severe, potentially life-threatening outcomes following traumatic brain injury. And cerebral vasospasm after subarachnoid hemorrhage could contribute to delayed cerebral ischemia. In addition, the role of neurovascular dysfunction in the major depressive disorder has also been identified. However, more inquiries need to be answered: i) The dynamic changes of neurovascular dysfunction following brain injuries? ii) The key mechanisms and therapeutic targets of such changes? iii) The crosstalk between the vascular system and other cells in the brain? The goal of this special issue is to highlight recent advances in the pathophysiology, diagnosis, and potential therapeutic targets of neurovascular changes following brain injuries. Original research contributing to medical translation and clinical observation/trials is welcome.
We would like to accept valuable manuscripts addressing any vascular events following diverse brain injuries (trauma, stroke, swelling, inflammation, infection), which include but are not limited to the following:
• Functional or structural remodeling of endothelial cells, smooth muscle cells, and pericytes
• Global or regional cerebral blood flow changes
• The crosstalk between the vascular system and other cells (neuron, glia, etc).
• Blood-brain barrier disruption and restoration
• Circular biomarkers predicting neurological outcome
Following brain injuries, the cross-talk between neurons, glia, and vascular elements is greatly disrupted. Emerging experimental investigations suggested vascular failure is one of the key pathogenic factors, which essentially underlies the damaging secondary events, featured in early capillary permeability disruption resulting in producing cerebral edema, inflammation, and secondary neuron death. At delayed phases, vascular remodeling, particularly in angiogenesis and enhanced endothelial-derived trophic factor secretion, may promote endogenous neurogenesis and neuronal repair. Hence, novel therapy targeting early and delayed neurovascular dysfunction might provide promising opportunities to improve clinical outcomes for patients following brain injuries.
Till now, our understanding of neurovascular dysfunction in brain injuries was greatly expanded. Blood-brain barrier disruption is associated with severe, potentially life-threatening outcomes following traumatic brain injury. And cerebral vasospasm after subarachnoid hemorrhage could contribute to delayed cerebral ischemia. In addition, the role of neurovascular dysfunction in the major depressive disorder has also been identified. However, more inquiries need to be answered: i) The dynamic changes of neurovascular dysfunction following brain injuries? ii) The key mechanisms and therapeutic targets of such changes? iii) The crosstalk between the vascular system and other cells in the brain? The goal of this special issue is to highlight recent advances in the pathophysiology, diagnosis, and potential therapeutic targets of neurovascular changes following brain injuries. Original research contributing to medical translation and clinical observation/trials is welcome.
We would like to accept valuable manuscripts addressing any vascular events following diverse brain injuries (trauma, stroke, swelling, inflammation, infection), which include but are not limited to the following:
• Functional or structural remodeling of endothelial cells, smooth muscle cells, and pericytes
• Global or regional cerebral blood flow changes
• The crosstalk between the vascular system and other cells (neuron, glia, etc).
• Blood-brain barrier disruption and restoration
• Circular biomarkers predicting neurological outcome