TRPC6 Depletion Results in Loss of Myocardin And Phenotypic Modulation In Vascular Smooth Muscle Cells
This activity was presented at 2020 VRIC as part of Abstract Session 1: Arterial Remodeling and Discovery Science for Venous Disease.
This research describes a novel, TRPC6-dependent pathway that regulates vascular smooth muscle cells phenotype. The results of this study may lead to mechanism-based therapies to reduce phenotypic switching, and thus mitigate neointimal hyperplasia, following vascular intervention.
Professional Practice Gap
The durability of interventions for peripheral and coronary arterial occlusive disease is currently limited. Neointimal hyperplasia is the major cause of early restenosis and failure of vascular bypass grafting, angioplasty, and stenting. Strategies that combat neointimal hyperplasia therefore have the potential to improve outcomes of vascular intervention.
To create a virtual environment for the exchange of basic and translational vascular science that stimulates thoughtful discussion and motivates participants to discover solutions to important problems affecting vascular patients.
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