FOXP1 and Myocardial fibrosis: The major findings of the present study were that EC-Klf2 signal mediates the inhibitory effects of simvastatin on pathological myocardial fibrosis and hypertrophy and improvement of cardiac dysfunction via direct suppression of TGFβ1 or through EC-Klf2-Foxp1-TGFβ1 pathway, thus revealing a novel cholesterol lowering independent mechanism for simvastatin in the prevention of cardiac dysfunction progression to HF during the process of myocardial remodeling in the TAC pressure overloading model.