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.

Knowledge Strategy
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. 

Learning Objectives

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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The opinions or views expressed on the SVS OnDemand platform and the SVS Video Library are those of the faculty and do not necessarily reflect the opinions, recommendations, or endorsement of SVS. Participants should critically appraise the information presented and are encouraged to consult appropriate resources for information surrounding any product or device mentioned. Information presented, as well as publications, technologies, products and/or services discussed, are intended to inform the learner about the knowledge, techniques, and experiences of SVS faculty who are willing to share such information with colleagues. The SVS disclaims any and all liability for damages to any individual user for all claims which may result from the use of said information, publications, technologies, products and/or services and events.

Course summary
Course opens: 
12/23/2020
Course expires: 
12/27/2024
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