Blocking potassium channels: a new principle for treating restenosis?

Abstract

This editorial refers to ‘Potent suppression of vascular smooth muscle cell migration and human neointimal hyperplasia by KV1.3 channel blockers’ by A. Cheong et al ., pp. 282–289, this issue. Vascular smooth muscle cells are important for the structural integrity of the tunica media, but they are also central to vascular remodelling in response to injury. Although they are highly differentiated cells with the ability to regulate vascular tone and synthesize extracellular matrix, smooth muscle cells are also very plastic cells. This enables them to switch from a contractile to an invasive, migrating, and proliferating phenotype in response to local injury. Ion channels in the plasmalemma of smooth muscle cells have been implicated in this active process. There is evidence of profound changes in the types of ion channels that are expressed or functionally important during vascular smooth muscle cell transition resulting in occlusive vascular pathologies. In the systemic circulation, vessel restenosis remains a major factor limiting the success of balloon angioplasty/stenting of coronary, carotid, and femoral arteries.1 A critical event seems to be replacement of the KCa1.1 (BKCa) with the intermediate-conductance Ca2+-activated potassium channel KCa3.12 and the loss of Cav1.2 (the L-type voltage-dependent) calcium channels.3 This event confers functional dominance on other types of calcium channels, including the channel components transient receptor potential (TRP) C(canonical)1, …