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Review
. 2014;21(18):2035-42.
doi: 10.2174/0929867321666131228223400.

Mechanisms of neurovascular dysfunction in acute ischemic brain

Y Terasaki, Y Liu, K Hayakawa, L D Pham, E H Lo, X Ji, K Arai  1
Affiliations
Review

Mechanisms of neurovascular dysfunction in acute ischemic brain

Y Terasaki et al. Curr Med Chem. 2014.

Abstract

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.

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Conflict of interest statement

CONFLICT OF INTEREST

The author(s) confirm that this article content has no conflicts of interest.

Figures

Fig. (1)
Fig. (1)
Neurovascular Unit (NVU) is composed with neurons, glia (astrocytes, microglia, and oligodendrocytes), vascular components (endothelial cells, pericytes, and smooth muscle cells), and extracellular matrix. Non-neuronal components have cell-cell interactions with neurons through endogenous molecules, such as cytokines, growth factors, chemokines, and microparticles. Neuronal function is maintained on the basis of mutual interactions, but after ischemic stroke, non-neuronal compartments may lead to neuronal damage, resulting in overall NVU/brain dysfunction.
See this image and copyright information in PMC

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