A TRPC3 blocker, Pyr3, prevents stent-induced arterial remodeling

Background TRPC-mediated Ca entry has been implicated in the control of smooth muscle proliferation and might represent a pivotal mechanism underlying in-stent restenosis. As we have observed significant expression of TRPC3 in human smooth muscle from coronary arteries as well as from aorta, we tested the efficiency of a recently discovered TRPC3-selective Ca entry blocker, Pyr3 (10 μM) to prevent vascular smooth muscle proliferation and stent implantation-induced hyperplasia of human aorta.