Document Detail

Pathophysiology of collateral development.
MedLine Citation:
PMID:  15492584     Owner:  NLM     Status:  MEDLINE    
The formation of collateral arteries in patients suffering from occlusive atherosclerotic vascular diseases has been frequently reported. The growth of these collateral arteries has been termed 'arteriogenesis'. Clinical observations and investigations using various animal models support the hypothesis that the mechanism of arteriogenesis is based on the remodelling of pre-existing collateral anastomoses. This process seems to be mainly triggered by fluid shear stress which is induced by the altered blood flow conditions after an arterial occlusion. Early arteriogenesis involves the activation of collateral endothelial cells, the attraction of leukocytes to the collateral vascular wall and subsequently their invasion into the perivascular space of the collateral vessel. In a second phase, proliferation of vascular cells is initiated by growth factors mainly released from accumulated leukocytes. Furthermore, tissue degradation and changes in the extracellular matrix are observed. Unravelling the mechanisms of arteriogenesis is crucial to the development of successful therapeutic approaches for the treatment of patients with ischemic vascular diseases.
Matthias Heil; Wolfgang Schaper
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Coronary artery disease     Volume:  15     ISSN:  0954-6928     ISO Abbreviation:  Coron. Artery Dis.     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-10-19     Completed Date:  2005-06-16     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9011445     Medline TA:  Coron Artery Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  373-8     Citation Subset:  IM    
Department of Experimental Cardiology, Max-Planck-Institute for Physiological and Clinical Research, Bad Nauheim, Germany.
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MeSH Terms
Collateral Circulation*
Neovascularization, Physiologic*
Vascular Diseases / physiopathology*

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