Abstract
Cellular proliferation requires an increase in expression and function of K+ channels.1–3 Blockade of K+ channels 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 proliferation, and selective blockade of these voltage-gated K+ channels inhibits proliferation.4 New research by the same group presented in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology further extends these findings to show that in both proliferating, cultured mouse smooth muscle cells and balloon-injured mouse arteries, expression of KV1.3 (locus: KCNE3 ) is upregulated …
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