We further demonstrated that the blockade of IL-17A inhibited atrial fibrosis and decreased the level of Col-1, Col-3 and α-SMA in the rats with SP, similar to the effects reported in models of cardiac infarction (9,11) and myocarditis-induced cardiac fibrosis (16), and consistent with a potential role for IL-17A in cardiac fibrosis (9,10,12). Here, ACTA1 is linked to myocarditis.