Moreover, in in vivo fibrosis models it was shown that Pyr3 treatment reduces the increase in proliferation and α-SMA expression observed in left atrial fibroblasts from an atrial fibrillation model in dogs [54], the cardiac fibrosis and expression of fibrosis associated genes after pressure overload, and the TGF-β-induced CTGF and αSMA expression in human fibroblasts [55]. This evidence concerns the gene TGFB1 and atrial fibrillation.