Abstract
Background and Aims: To date, no effective pharmacological therapy has proven to halt or delay the progression of calcific aortic valve disease (CAVD). We aimed to investigate the effects of the activation of Formyl Peptide Receptor 2 (FPR2), a known receptor for lipoxins, resolvins and anti-inflammatory molecules, on interstitial aortic valve cells (VICs) calcification.
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