doi: 10.1161/CIRCRESAHA.108.173021
© 2008 American Heart Association, Inc.
Editorials |
Physics Meets Molecules
Is Modulation of Shear Stress the Link to Vascular Prevention?
From Art.Net. (Arteriogenesis Network), Universitätsmedizin Berlin-Charité, Center for Cardiovascular Research, Department for Internal Medicine, CC 13 Cardiology, Berlin, and University Clinic Freiburg-Cardiology, Freiburg; and the Max Delbrück Center for Molecular Medicine, Department of Angiogenesis and Cardiovascular Pathology, Germany.
Correspondence to Universitätsmedizin Berlin-Charité, Center for Cardiovascular Research CCR, CC 13, Hessische Strasse 3-4, 10115 Berlin, Germany. E-mail ivo.buschmann@charite.de
See related article, pages 538–545
Key Words: shear stress • arteriogenesis • collateral arteries • cardiovascular prevention
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Arteries and veins are permanently exposed to hemodynamic forces because of the pulsatile nature of blood pressure and flow. Hence, the endothelium is constantly detecting different biomechanical forces, cyclic stretch and shear stress in particular,1–2 and converts the latter stimuli into intra- and extracellular signals. Endothelial cells thereby modulate multiple of physiological and pathophysiological processes: production of growth-promoting and growth-inhibiting hormones, enzymes, cytokines, etc; mediation of inflammatory responses through the expression of chemotactic and adhesion molecules on the endothelial surface; modulation of hemostasis and thrombosis via secretion of procoagulant, anticoagulant, and fibrinolytic agents; and the regulation of vascular smooth muscle cell contraction through the release of vasodilators and vasoconstrictors.3–5
This being the case, the equilibrium between physiological levels of blood flow (shear stress) and the endothelium is tightly counterbalanced. Thereby, the lumen radius of an artery is the most important denominator, which signifies that the smaller the lumen the higher the shear stress. However, once physiological shear forces are reduced, several pathological conditions may arise: proatherogenic and/or prothrombotic states and hence atherosclerosis and/or thrombosis.6–7 Inversely, high levels of shear forces play a key role in adaptive phases of arteriogenesis (collateral artery growth), the most clinically relevant mechanism of vascular development.8 In case of an arterial stenosis, these arterial/arteriolar anastomoses are the only anastomosis to the low-pressure territory and perfuse the periphery with nutrient blood flow. Elevation of shear stress and concomitant cyclic stretch are currently discussed to be the strongest inducers of arteriogenesis. In a rabbit model of femoral artery
Related Article:
Circ. Res. 2008 102: 538-545.