What is the vascular smooth muscle cell

The vascular smooth-muscle cell, the major cell type of the media layer of blood vessels, also contributes actively to vascular
pathobiology. Contraction and relaxation of smooth-muscle cells at the level of the muscular arteries controls blood pressure, and,
hence, regional blood flow and the afterload experienced by the left ventricle (see below). The vasomotor tone of veins, which is

governed by smooth-muscle cell tone, regulates the capacitance of the venous tree and influences the preload experienced by both
ventricles. Smooth-muscle cells in the adult vessel seldom replicate. This homeostatic quiescence of smooth-muscle cells changes in
conditions of arterial injury or inflammatory activation. Proliferation and migration of arterial smooth-muscle cells, which is associated
with a change in phenotype characterized by lower content of contractile proteins and greater production of extracellular matrix
macromolecules, can contribute to the development of arterial stenoses in atherosclerosis, arteriolar remodeling that can sustain
and propagate hypertension, and the hyperplastic response of arteries injured by angioplasty or stent deployment. In the pulmonary
circulation, smooth-muscle migration and proliferation contribute decisively to the pulmonary vascular disease that gradually occurs
in response to sustained high-flow states such as left-to-right shunts. Such pulmonary vascular disease provides a major obstacle to
the management of many patients with adult congenital heart disease. Elucidation of the signaling pathways that regulate the
reversible transition of the vascular smooth-muscle cell phenotype remains an active focus of investigation. Among other mediators,
microRNAs have emerged as powerful regulators of this transition, offering new targets for intervention.
The activated, phenotypically modulated smooth-muscle cells secrete the bulk of vascular extracellular matrix. Excessive production
of collagen and glycosaminoglycans contributes to the remodeling and altered biology and biomechanics of arteries affected by
hypertension or atherosclerosis. In larger elastic arteries, the elastin synthesized by smooth-muscle cells serves to maintain not only
normal arterial structure but also hemodynamic function. The ability of the larger arteries, such as the aorta, to store the kinetic
energy of systole promotes tissue perfusion during diastole. Arterial stiffness associated with aging or disease, as manifested by a
widening pulse pressure, increases left ventricular afterload and portends a poor outcome.
Like endothelial cells, vascular smooth-muscle cells do not merely respond to vasomotor or inflammatory stimuli elaborated by other
cell types but can themselves serve as a source of such stimuli. For example, when exposed to bacterial endotoxin or other
proinflammatory stimuli, smooth-muscle cells can elaborate cytokines and other inflammatory mediators. Like endothelial cells, upon
inflammatory activation, arterial smooth-muscle cells can produce prothrombotic mediators such as tissue factor, the antifibrinolytic
protein PAI-1, and other molecules that modulate thrombosis and fibrinolysis. Smooth-muscle cells also elaborate autocrine growth