Smooth muscle cells and vascular diseases

Vascular smooth muscle cells (VSMCs) are the stromal cells of the vascular wall, and, due to their myosin/actin interactions, they are also responsible for arterial contractile tonus and regulating blood pressure and flow in relation to specific metabolic demands. VSMCs show considerable differences depending on their position in the arterial tree (large conduit vs. small resistance vessels), their embryologic origin, and their organ-dependent microenvironment; the heart, brain, kidney, etc. As the stromal cells of the arterial wall, VSMCs synthesize and secrete insoluble extracellular matrix (ECM) molecules that assume the function of withstanding the high pressure of the circulating blood in the arterial system. For example, totally decellularized aortic grafts, created using sodium dodecyl sulphate detergent, are experimentally able to resist arterial blood pressure in the aorta in vivo , without dilating.1 This mechanical function predominates in large vessels, since pressure-dependent stress of the wall is also dependent on the diameter.2 Therefore, cell–ECM interactions are of particular importance in these large arteries. The contractile tonus of VSMCs, dependent on sympathetic innervation, is responsible for the peripheral resistance to blood flow generated by the beating heart, leading to the genesis of blood pressure. This function is mainly the characteristic of resistance arteries and arterioles and involves cell–cell interactions.Due to pressure-dependent radial hydraulic conductance, the arterial wall is constantly submitted to outward convection of circulating plasma molecules.3 This physiological outward convection of plasma peptides or macromolecules is the main source of extrinsic stimuli, which, with time, cause damage to arterial VSMCs (pressure-dependent strain, lipid overload, hyperglycaemia, zymogens). In response to changes in their plasma-dependent microenvironment, VSMCs may either die or adapt, modifying their phenotype through acute, ligand/receptor-dependent signalling pathways or chronic nuclear signalling involving epigenetic molecular remodelling of their nuclear chromatin. VSMCs can also be the target of intrinsic …