Kv3.4, a key signalling molecule controlling the cell cycle and proliferation of human arterial smooth muscle cells

Abstract

This editorial refers to ‘Cell cycle-dependent expression of Kv3.4 channels modulates proliferation of human uterine artery smooth muscle cells’ by E. Miguel-Velado et al. , pp. 383–391, this issue. Smooth muscle cells, in contrast to their fully differentiated striated muscle counterparts, display the remarkable property of being able to alter their phenotype in response to environmental changes. Upon exposure to physiological (e.g. hormones, growth factors, etc.) or pathophysiological (e.g. low oxygen tension, mitogenic factors, acidosis) stimuli, vascular smooth muscle cells (VSMCs) can switch their phenotype from a normal contractile state to a non-contractile, proliferative, and migratory behaviour that plays a prime function in the structural remodelling of blood vessels. This phenotypic switch is most often detrimental in disease states since the partial or complete obstruction of the lumen by thickening of the muscle layer or media causes ischaemia and impaired perfusion of the tissue.1–3 The so-called 'plasticity' of VSMCs1 has been the subject of intense investigation as it was recognized early to play an important role in the initiation and progression of common human vascular disorders such as systemic and pulmonary hypertension, ischaemic heart disease and stroke, and restenosis following coronary arterial angioplasty.3 The switch from a contractile to a proliferative state is … *Corresponding author. Tel: +1 775 784 1420; fax: +1 775 784 1620, Email: nleblanc{at}medicine.nevada.edu