Abstract

Background and Aims : We previously showed that female key driver genes are involved in vascular smooth muscle cell plasticity in female atherosclerotic plaques. To further study mechanisms on how those sex-driven genes contribute to atherosclerotic disease they need to be first prioritized in a relevant in vitro model system. We hypothesize that human isolated plaque cells retain diseased key driver gene expression and activity and therefore can be used for plasticity experiments to prioritize and study the function of female key driver genes.

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