Stroke is the third leading cause of morbidity and long-term disability. Reestablishment of functional microvasculature such as promotion of angiogenesis and arteriogenesis in the ischemic border creates a hospitable microenvironment for neuronal plasticity leading to functional recovery. To capitalize on angiogenesis and arteriogenesis as therapeutic targets for stroke treatment, knowledge of the precise molecular mechanisms which stimulate these vascular processes is necessary. Vascular endothelial growth factor, its receptors, the Angiopoietin-1 (Ang1)/Tie2 system and endothelial nitric oxide synthase, among other angiogenic factors mediate and contribute to post-ischemic angiogenesis and arteriogenesis. This chapter reviews molecular mechanisms which promote angiogenesis and arteriogenesis following cerebral ischemia and the associated vascular remodeling effects of experimental pharmacological (Statins and Niaspan) and cellular (bone marrow stromal cells) approaches for the treatment of stroke.
CITATION STYLE
Chen, J., & Chopp, M. (2012). Angiogenesis and arteriogenesis as stroke targets. In Translational Stroke Research: From Target Selection to Clinical Trials (pp. 231–249). Springer New York. https://doi.org/10.1007/978-1-4419-9530-8_11
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