Cell Biochemistry and Biophysics

, Volume 43, Issue 1, pp 1–15

The art of arteriogenesis

Original Article

DOI: 10.1385/CBB:43:1:001

Cite this article as:
Deindl, E. & Schaper, W. Cell Biochem Biophys (2005) 43: 1. doi:10.1385/CBB:43:1:001


The identification of collateral artery growth (arteriogenesis) as the only mechanism to compensate for the loss of an occluded artery forced us to define the mechanisms responsible for this type of vessel growth. To achieve this, a variety of coronary as well as peripheral models of arteriogenesis have been developed. Based on these studies it is obvious that arteriogenesis obeys different mechanisms than angiogenesis, the sprouting of capillaries. Upon occlusion of an artery, the blood flow is redirected into preexisting arteriolar anastomoses that experience increased mechanical forces such as shear stress and circum ferential wall stress. The endothelium of the arteriolar connections is then activated, resulting in an increased release of monocyte-attracting proteins as well as an upregulation of adhesion molecules. Upon adherence and extravasation, monocytes promote arteriogenesis by supplying growth factors and cytokines that bind to receptors that are expressed on vascular cells within a limited time frame. Animal studies evidenced that factors, such as monocyte chemoattractant protein-1, granulocyte-monocyte colony-stimulating factor, or transforming growth factor-β1, that either attract or prolong the lifetime of monocytes efficiently enhance collateral artery growth, an effect that was seen only to a minor degree after application of a single growth factor. Bone marrow-derived stems cells and endothelial progenitor cells do not incorporate in growing arteries but, rather, function as supporting cells. Complete elucidation of the mechanisms of arteriogenesis may lead to efficacious therapies counteracting the devastating consequences of vascular occlusive diseases.

Index Entries

Arteriogenesis collateral arteries monocytes mechanical forces hypoxia stem cells vascular endothelial growth factor fibroblast growth factor urokinase plasminogen activator cofilin 

Copyright information

© Humana Press Inc 2005

Authors and Affiliations

  1. 1.Klinikum Grosshadern, Medical Clinic 1Ludwig-Maximilians-UniversityMunichGermany
  2. 2.Department of Experimental CardiologyMax-Planck-Institute for Physiological and Clinical ResearchBad NauheimGermany

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