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Circulation Research. 2004;94:573-574
doi: 10.1161/01.RES.0000124603.46777.EB
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(Circulation Research. 2004;94:573.)
© 2004 American Heart Association, Inc.


Editorials

A Different Outlook on the Role of Bone Marrow Stem Cells in Vascular Growth

Bone Marrow Delivers Software not Hardware

Matthias Heil, Tibor Ziegelhoeffer, Barend Mees, Wolfgang Schaper

From the Max-Planck-Institute for Physiological and Clinical Research (M.H., T.Z., W.S.) and Kerckhoff-Clinic (T.Z.), Bad Nauheim, Germany; and Departments of Vascular Surgery and Cell Biology and Genetics (B.M.), Erasmus Medical Center, Rotterdam, the Netherlands.

Correspondence to Prof Dr med Wolfgang Schaper, Max-Planck- Institute for Physiological and Clinical Research, Department of Experimental Cardiology, Benekestrasse 2, 61231 Bad Nauheim, Germany. E-mail w.schaper@kerckhoff.mpg.de


Key Words: arteriogenesis • bone marrow • vascular growth • cytokines


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Blood vessel growth in adult organisms is a process occurring under various physiological and pathological conditions. Two forms of blood vessel growth have been described after birth: angiogenesis, ie, capillary sprouting, and arteriogenesis, ie, growth of large conductance arteries from preexisting arterial anastomoses (collaterals).1,2 It is increasingly recognized that blood flow deficits caused by occlusion or stenosis of a major artery can only be efficiently compensated by arteriogenesis.

Fluid shear stress (FSS) is suggested to be the molding force for arteriogenesis. The activation of the collateral endothelium caused by increased FSS is reflected by an upregulation of adhesion molecules and release of cytokines that attract circulating blood cells, mainly monocytes, to adhere to and invade the collateral vessel wall.3 Besides this monocyte/macrophage accumulation around growing collaterals, also an increase in numbers of T cells and granulocytes has been reported, underlining the paradigm that circulating cells are of a great importance in this type of vascular growth.4,5 A variety of different cytokines and proteases (ie, MCP-1, FGF-2, TGF-ß, uPA, and MMPs) produced by these invading cells have been identified to stimulate endothelial and smooth muscle cell proliferation and migration as well as tissue degradation.6 This has led to a number of animal studies and clinical phase I trials demonstrating the short-term safety of administering several cytokines. However, recent clinical phase II trials have failed to extrapolate the promising results from animal studies into the therapeutic realm in human patients.7,8

New therapeutic approaches to promote arteriogenesis have evolved when it was suggested . . . [Full Text of this Article]




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