The cerebrovasculature is a highly specialized vascular network that possesses many unique functions, such as supplying oxygen and nutrients to meet the extremely high metabolic demand of brain tissue as well as building a blood-brain barrier (BBB) to protect sensitive neurons from toxic metabolites and xenobiotics in the circulation. Currently, acute cerebrovascular dysfunction including ischemic and hemorrhagic stroke is a leading cause of human death and disability worldwide. Furthermore, even in the absence of acute disease, chronic cerebrovascular dysfunction, such as BBB disruption, endothelial dysfunction, or microvessel regression, is associated with or underlie the pathogenesis and progression of many neurological disorders, including neuroinflammation, aging-related cognition decline, Alzheimer’s disease, Multiple Sclerosis, brain tumors, epilepsy, etc.
The homeostasis of the cerebrovascular function is critically regulated by the neurovascular unit (NVU), which is composed of neuronal cells and non-neuronal cells including endothelial cells, vascular mural cells, astrocytes, and microglia. These cellular components are closely associated and interact with each other to regulate the growth, stability, and permeability of the cerebrovasculature. Dysregulation of any of these cellular components or the cross-talks between them may cause cerebrovascular dysfunction, which leads to neurological function impairment. Despite significant advances that have been made in this field, there remains an overt lack of comprehensive understanding of the cellular mechanism of cerebrovasculature and its role in the regulation of neuronal function under both physiological and pathophysiological conditions.
In this research topic, we welcome authors to submit Original Research, Review and Perspective articles related to the physiology of cerebrovascular function, pathology of chronic cerebrovascular dysfunction, and how cerebrovasculature regulates the neuronal cells. Studies using animal models or cell models are both welcomed. We anticipate that this special issue will underline the cellular mechanisms of cerebrovascular dysfunction and its critical role in neurological disorders, and attract broad interests for further research in this topic.
Potential topics include but are not limited to the following:
1) Investigating the key factors and pathways involving in the regulation of cerebrovascular structure and function (endothelial function, angiogenesis, NVU and BBB formation, and integrity, etc.) under homeostatic and pathological conditions.
2) Studying the cellular mechanism of cerebrovascular dysfunction using novel experimental models.
3) Discovering therapeutic targets and approaches to modulate these targets that aim to improve cerebrovascular dysfunction and related neurological deficits.
4) Identifying the impact of cerebrovascular dysfunction on neuronal cells and the underlying mechanism.
The cerebrovasculature is a highly specialized vascular network that possesses many unique functions, such as supplying oxygen and nutrients to meet the extremely high metabolic demand of brain tissue as well as building a blood-brain barrier (BBB) to protect sensitive neurons from toxic metabolites and xenobiotics in the circulation. Currently, acute cerebrovascular dysfunction including ischemic and hemorrhagic stroke is a leading cause of human death and disability worldwide. Furthermore, even in the absence of acute disease, chronic cerebrovascular dysfunction, such as BBB disruption, endothelial dysfunction, or microvessel regression, is associated with or underlie the pathogenesis and progression of many neurological disorders, including neuroinflammation, aging-related cognition decline, Alzheimer’s disease, Multiple Sclerosis, brain tumors, epilepsy, etc.
The homeostasis of the cerebrovascular function is critically regulated by the neurovascular unit (NVU), which is composed of neuronal cells and non-neuronal cells including endothelial cells, vascular mural cells, astrocytes, and microglia. These cellular components are closely associated and interact with each other to regulate the growth, stability, and permeability of the cerebrovasculature. Dysregulation of any of these cellular components or the cross-talks between them may cause cerebrovascular dysfunction, which leads to neurological function impairment. Despite significant advances that have been made in this field, there remains an overt lack of comprehensive understanding of the cellular mechanism of cerebrovasculature and its role in the regulation of neuronal function under both physiological and pathophysiological conditions.
In this research topic, we welcome authors to submit Original Research, Review and Perspective articles related to the physiology of cerebrovascular function, pathology of chronic cerebrovascular dysfunction, and how cerebrovasculature regulates the neuronal cells. Studies using animal models or cell models are both welcomed. We anticipate that this special issue will underline the cellular mechanisms of cerebrovascular dysfunction and its critical role in neurological disorders, and attract broad interests for further research in this topic.
Potential topics include but are not limited to the following:
1) Investigating the key factors and pathways involving in the regulation of cerebrovascular structure and function (endothelial function, angiogenesis, NVU and BBB formation, and integrity, etc.) under homeostatic and pathological conditions.
2) Studying the cellular mechanism of cerebrovascular dysfunction using novel experimental models.
3) Discovering therapeutic targets and approaches to modulate these targets that aim to improve cerebrovascular dysfunction and related neurological deficits.
4) Identifying the impact of cerebrovascular dysfunction on neuronal cells and the underlying mechanism.