Editorial KV1.3 A New Therapeutic Target to Control Vascular Smooth Muscle Cell

Cellular proliferation requires an increase in expressionand function of K channels.1–3 Blockade of K chan-nels inhibits proliferation of many cell types,1,3 including vascular smooth muscle cells.2,4–7 Previous studies have shown growth factor-induced upregulation of KCa3.1 (sK4, IK1, locus KCNN4) in cultured smooth muscle cells; selective inhibition of these channels reduces smooth muscle cell proliferation.2,6,7 Importantly, KCa3.1 blockers also attenuate restenosis after balloon injury in rat7 and pig8 models, and they limit atherogenesis in a mouse model of this disease.9 However, KCa3.1 does not appear to be the only K channel that can function in this role. In human uterine artery smooth muscle cells, KV3.4 (locus: KCNC4) appears to function similarly, as its expression is upregulated during prolifera-tion, and selective blockade of these voltage-gated K channels inhibits proliferation.4 New research by the sam