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Vascular remodelling in physiology and disease is substantially due to vascular smooth muscle cells and endothelial cells that switch to phenotypes characterised by proliferation, migration, secretion, invasion etc.We have sought to understand ion channels in this context, particularly in human diseased tissue.Data are consistent with roles of the potassium channels KCa3.1 and Kv1.3.Most of our recent work has, however, focused on calcium-permeable channels that are chemically activated.The data suggest that the TRPC1 channel subunit has an important role and is up-regulated in remodelling.Intriguingly, it inhibits the function of other TRPC channels and yet drives calcium entry and remodelling.We have shown that TRPC 1 operating with TRPC5 is stimulated by oxidized phospholipids, key players in atherosclerosis (AL-Shawafet al 2010, ATVB 30, 1453-).Other types of calcium channel also contribute, probably in coordination with TRPC channels.Data suggest roles for Orail and STIM1 as subunits/regulators of CRAC channels.Signaling by growth factors such a PDGF and VEGF shows striking dependence on such channels, conferring functional significance for cell migration and angiogenesis (Li et al 2011, Circ Res published on-line).These and other recent findings will be discussed.Financial support is provided by the Wellcome Trust, British Heart Foundation, Medical Research Council.