Xing Changhong, Hayakawa Kazuhide, Lok Josephine, Arai Ken, Lo Eng H
Neuroprotection Research Laboratory, Massachusetts General Hospital, Boston, USA.
Neurol Res. 2012 May;34(4):325-30. doi: 10.1179/1743132812Y.0000000019.
The neurovascular unit provides a conceptual framework for investigating the pathophysiology of how brain cells die after stroke, brain injury, and neurodegeneration. Emerging data now suggest that this concept can be further extended. Cell-cell signaling between neuronal, glial, and vascular elements in the brain not only mediates the mechanisms of acute injury, but integrated responses in these same elements may also be required for recovery as the entire neurovascular unit attempts to reorganize and remodel. Understanding the common signals and substrates of this transition between acute injury and delayed repair in the neurovascular unit may reveal useful paradigms for augmenting neuronal, glial, and vascular plasticity in damaged and diseased brain.
神经血管单元为研究中风、脑损伤和神经退行性变后脑细胞死亡的病理生理学提供了一个概念框架。新出现的数据表明,这一概念可以进一步扩展。大脑中神经元、神经胶质细胞和血管成分之间的细胞间信号传导不仅介导急性损伤机制,而且当整个神经血管单元试图重组和重塑时,这些相同成分中的整合反应对于恢复可能也是必需的。了解神经血管单元中急性损伤和延迟修复之间这种转变的共同信号和底物,可能会揭示增强受损和患病大脑中神经元、神经胶质细胞和血管可塑性的有用范例。