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Physical, Cellular & Molecular Mechanisms of Collateral Artery Growth
Author(s) -
Heil Matthias
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.520.4
Subject(s) - arteriogenesis , collateral circulation , anatomy , artery , extracellular matrix , microbiology and biotechnology , ischemia , cardiology , medicine , chemistry , biology
The compensatory growth of blood vessels after major arterial occlusions has been termed arteriogenesis. Arteriogenesis describes the remodelling of small interconnecting arterial anastomoses with almost no net blood flow to large functional arteries. It has been shown that growth of these collateral arteries is triggered by physical forces, but does not require hypoxia as a stimulus. Using a hind limb ischemia model in combination with an arterio‐venous shunt the role of chronically increased fluid shear stress (FSS) was investigated. FSS initiates the activation of endothelial cells and modulates processes, which control attraction of circulating cells to the collateral wall. On the molecular level, a number of genes was found to be induced by FSS. Moreover, monocytes were shown to have a pivotal role for arteriogenesis. After entering the vascular wall they function as micro‐bioreactors producing cytokines, thereby controlling cell proliferation and remodelling. Cell proliferation coincides with the transient dismantling of extracellular structures by proteases. After the re‐arrangement of wall structures collaterals with large calibres represent functional arteries