These changes were associated with increased cardiac profibrotic M2-macrophage population, TGFβ secretion, phosphorylation of Smad2 and -3, fibroblast activation, expression of FN1 and LOX, and myocardial fibrosis (Figs. 5 and 6). This evidence concerns the gene TGFB1 and Myocardial fibrosis.