From INSERM U141, Paris, France.
Correspondence to Alain Tedgui, INSERM U141, 41 Blvd de la Chapelle, 75475 Paris, Cedex 10, France. E-mail tedgui{at}infobiogen.fr
Abstract
Abstract—The vascular wall is
constantly subjected to a variety of mechanical forces in the form of
stretch (tensile stress), due to blood pressure, and shear stress, due
to blood flow. Alterations in either of these stresses are known to
result in vascular remodeling, an adaptation characterized by modified
morphology and function of the blood vessels, allowing the vessels to
cope with physiological or pathological conditions.
The processes involved in vascular remodeling include cellular
hypertrophy and hyperplasia, as well as enhanced protein
synthesis or extracellular matrix protein reorganization. In vitro
studies using vascular cells have attempted to identify the mechanisms
behind structural alterations. Possible pathways include ion channels,
integrin interaction between cells and the extracellular matrix,
activation of various tyrosine kinases (such as c-Src, focal adhesion
kinase, and mitogen-activated protein kinases), and autocrine
production and release of growth factors. These pathways lie
upstream of de novo synthesis of immediate response genes and total
protein synthesis, both of which are likely to be involved in the
process of vascular remodeling.
© 1998 American Heart Association, Inc.
Third Workshop on Structure and Function of Large Arteries: Part II
Signal Transduction of Mechanical Stresses in the Vascular Wall
Key Words: shear stress • stretch • muscle, smooth • endothelium • MAP kinases
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