Post-stroke Blood-brain Barrier Research Articles

In Vivo Imaging of Neurovascular Remodeling After Stroke

Stroke is one of the leading causes of adult disability throughout the world and, even though neural mechanisms of loss of function have been extensively studied, many aspects of poststroke cerebral responses remain poorly understood. Of particular interest is the mounting evidence of the capacity of the adult brain to reorganize after injury, which is believed to contribute to limitation of the extent of neural dysfunction and to restoration of affected neural functions. Processes such as neuronal plasticity, glial proliferation, and neovascularization may be essential for preservation or recovery of function after stroke and may conceivably go hand-in-hand at nearby and remote sites of active tissue reorganization.1,2 Specifically, the acute initiation of neurovascular remodeling, stimulating the proliferation and growth of existing arteries/arterioles (ie, arteriogenesis) or new capillaries (ie, angiogenesis), may be critical to facilitate the survival and restructuring of neural tissue, which ultimately may contribute to functional recovery at later stages.3 A variety of vascular imaging strategies is available for in vivo detection, characterization, and quantification of these processes, which can significantly aid in elucidation of the role of neurovascular remodeling after stroke, as discussed in this review. Because most of the described imaging modalities are present in experimental and clinical settings, this raises significant opportunities for translational studies. Growth and remodeling of existing and nascent vascular networks in health and disease involve a number of critical steps that have been comprehensively described by Risau4 and Carmeliet.5 Arteriogenesis involves adaptive growth and proliferation of preexisting (collateral) arteries and arterioles in response to increase in intravascular shear forces. The increased shear stress leads to upregulation of cell adhesion molecules, followed by accumulation of monocytes and other leukocytes that release cytokines and growth factors around the proliferating and maturating arteries.6 Although arteriogenic growth of collateral …