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A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
Published on: November 19, 2019
Cerebrovascular inflammation: A critical trigger for neurovascular injury?
Muhammad Naveed1, Qi-Gang Zhou2, Feng Han1
1Key Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, Jiangsu Province, PR China.
Abstract:
The cerebrovascular system is not only inert bystandard that support the metabolic demands of the brain but also elicit the barrier functions against risk factors mediated neurovascular injury. The onsets of cerebrovascular inflammation are considered as stimuli that can provoke the host defense system and trigger the development of neurological disorders. Homeostasis of the brain function is regulated by the movement of endothelial, glial, and neuronal cells within the neurovascular unit (NVU), which acts as a "platform" for the coordinated action of anti- and pro-inflammatory mechanisms. The cerebrovascular system plays an integral role in the inflammatory response by either producing or expressing a variety of cytokines, adhesion molecules, metalloproteinases, and serine proteases. Excessive inflammatory cytokine production can further be affecting the blood-brain barrier (BBB) integrity and lead to brain tissue damage. In this review, we summarize the more recent evidence highlighting the importance of cerebrovascular injury in terms of risk prediction, and the mechanisms mediating the upregulation of inflammatory mediators in cerebrovascular dysfunction and neurodegeneration.
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