Terasaki Y, Liu Y, Hayakawa K, Pham L D, Lo E H, Ji X, Arai K
Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, USA.
Curr Med Chem. 2014;21(18):2035-42. doi: 10.2174/0929867321666131228223400.
The neurovascular unit is now well accepted as a conceptual framework for investigating the mechanisms of ischemic stroke. From a molecular and cellular perspective, three broad mechanisms may underlie stroke pathophysiology--excitotoxicity, oxidative stress and inflammation. To date, however, most investigations of these basic mechanisms have focused on neuronal responses. In this mini-review, we ask whether these mechanisms of excitotoxicity, oxidative stress and inflammation can also be examined in terms of non-neuronal interactions in the neurovascular unit, including the release of extracellular vesicles for cell-cell signaling.
神经血管单元现已被广泛接受为研究缺血性中风机制的概念框架。从分子和细胞角度来看,中风病理生理学可能存在三种主要机制——兴奋性毒性、氧化应激和炎症。然而,迄今为止,对这些基本机制的大多数研究都集中在神经元反应上。在这篇小型综述中,我们探讨这些兴奋性毒性、氧化应激和炎症机制是否也可以从神经血管单元中的非神经元相互作用方面进行研究,包括用于细胞间信号传导的细胞外囊泡的释放。