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Cerebrovascular inflammation: A critical trigger for neurovascular injury?

机译:脑血管炎症:神经血管损伤的关键触发?

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摘要

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.
机译:脑血管系统不仅惰性标准,支持大脑的代谢需求,而且引起对患有神经血管损伤的风险因素的障碍功能。脑血管炎症的持续膜被认为是可以引发宿主防御系统的刺激,并引发神经系统疾病的发展。脑功能的稳态是由神经血管单元(NVU)内的内皮,胶质和神经元细胞的运动来调节,其作为抗炎症机制的协调作用的“平台”起作用。脑血管系统通过产生或表达各种细胞因子,粘附分子,金属蛋白酶和丝氨酸蛋白酶在炎症反应中起着积分作用。过量的炎症性细胞因子产生可以进一步影响血脑屏障(BBB)完整性并导致脑组织损伤。在这篇综述中,我们总结了最近的证据,突出了脑血管损伤在风险预测方面的重要性,以及调解脑血管功能障碍和神经变性的炎症介质上调的机制。

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