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Abstract
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.
This work is supported by grants from the American Heart Association and NINDS. Some concepts discussed here are based in part on data and ideas presented in previous reviews (Lok et al., Neurochem Res. 2007; Lo, Br J Pharmacol. 2008; Lo, Nat Med. 2008; Arai et al, FEBS J. 2009; Hayakawa et al., Ann New York Acad Sci. 2010; Lo, Nat Med. 2010; Moskowitz et al., Neuron. 2010).