Abstract
IFN-gamma is a recognized culprit of atherogenesis. Blockade of IFN-gamma signaling in vascular cells should positively impact intimal hyperplasia. Expression of STAT1, the key transcriptional regulator of IFN-gamma signaling, is regulated by autocrine IFN-beta. In turn, IFN-beta is downstream to the noncanonical I Kappa B kinase, TBK1. Our first aim was to validate, in vitro, the TBK1 inhibitor drug, amlexanox, and evaluate whether it reduces STAT1 expression, and thus, IFN-gamma signaling in vascular cells.
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