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Abstract Dioxins are persistent environmental pollutants found in industrial emissions, tobacco smoke, and air pollution. Chronic exposure is associated with cardiovascular disease, but how dioxins act within the vessel wall to promote atherosclerosis remains unclear. We aimed to determine how dioxin exposure alters vascular smooth muscle cell behavior and whether smooth muscle cell aryl hydrocarbon receptor signaling modifies plaque progression.
Abstract Vascular smooth muscle cells contribute to heritable coronary artery disease risk and undergo complex transitions to multiple disease-related phenotypes. To investigate the genetic basis of these trajectories, we develop a dense timecourse single-cell transcriptomic and epigenetic map of atherosclerosis in a murine disease model accompanied by high-plex in situ spatial data.
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1111/cts.13608.
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