Moreover, arjunolic acid as a Peroxisome Proliferator-Activated Receptorα (PPARα) agonist up-regulates PPARα, leading to repression of TGF-β signaling, especially by inhibiting TGF-β activated kinase1phosphorylation, which reduces the activity of p38MAPK and NFκBp65, ultimately reversing hypertrophy-related myocardial fibrosis. This evidence concerns the gene TGFB1 and Myocardial fibrosis.