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, a Novel Mediator of Strain-Induced Vascular Remodeling
From the Department of Medicine II, University of Giessen Lung Center, Justus Liebig University Giessen, Germany.
Correspondence to Oliver Eickelberg, MD, University of Giessen Lung Center, Department of Medicine II, Aulweg 123, Rm 6-11, D-35392 Giessen, Germany. E-mail oliver.eickelberg@innere.med.uni-giessen.de
See related article, pages 434441
Key Words: TGF-
ROS NADPH oxidase
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Blood vessels are continuously subjected to dynamic mechanical forces, including stretch and shear stress that increase with elevated blood flow, pressure, or viscosity. Under physiological conditions, eg, during vascular development, mechanical stress in the arterial wall regulates critical parameters of vascular function and thus plays a crucial role in keeping the balance between blood supply and tissue oxygen demand. Several protective mechanisms have evolved to maintain the physiological integrity and structure of vessels, such as adaptive changes of the vasomotor tone. In contrast to these physiological processes, sustained or chronic alterations in blood pressure and/or flow frequently lead to irreversible phenotypic changes of the vascular wall and finally vascular remodeling.1,2
The process of vascular remodeling is characterized by increased vascular smooth muscle cell (VSMC) growth, migration, and extracellular matrix deposition, as well as altered secretion of fibrotic growth factors by endothelial cells (EC).24 Ultimately, these mechanisms are responsible for impaired vessel relaxation, sustained vasoconstriction, and vascular inflammation in diseases such as atherosclerosis and coronary artery disease. Taken together, these phenomena present as key contributors of decreased lumen size, increased vessel resistance, and account for the process of vascular remodeling.
Although the structural changes that are induced by mechanical forces have been elucidated nicely in the past, particular attention has now focused on the plethora of signaling cascades that initiate and perpetuate the vascular remodeling process in response to strain. Cascades that have been investigated recently include reactive oxygen species (ROS),5 nitric oxide (NO),6 nuclear factor
B (NF-
B),7,8 epidermal growth
Related Article:
Mediates Nuclear Factor
B Activation in Strained Arteries
Circ. Res. 2006 99: 434-441.
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