Angiogenesis after cerebral ischemia.
Though the vascular system of the adult brain is extremely stable under normal baseline conditions, endothelial cells start to proliferate in response to brain ischemia. The induction of angiogenesis, primarily in the ischemic boundary zone, enhances oxygen and nutrient supply to the affected tissue. Additionally, the generation of new blood vessels facilitates highly coupled neurorestorative processes including neurogenesis and synaptogenesis which in turn lead to improved functional recovery. To take advantage of angiogenesis as a therapeutic concept for stroke treatment, the knowledge of the precise molecular mechanisms is mandatory. Especially, since a couple of growth factors involved in post-ischemic angiogenesis may have detrimental adverse effects in the brain by increasing vascular permeability. This article summarizes the knowledge of molecular mechanisms of angiogenesis following cerebral ischemia. Finally, experimental pharmacological and cellular approaches to stimulate and enhance post-ischemic angiogenesis are discussed.
Beck
Heike
H
Institute of Cardiovascular Physiology, Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians University Munich, Marchioninistr. 27, 81377, Munich, Germany. Heike.Beck@med.uni-muenchen.de
Plate
Karl H
KH
D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000473:pathology* / Q000503:physiopathology; D055495:Neurogenesis; D020127:Recovery of Function; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
D036341:Intercellular Signaling Peptides and Proteins; D042461:Vascular Endothelial Growth Factor A