It was previously demonstrated that the sesquiterpene compound could attenuate myocardial fibrosis by suppressing the TGF-β1/Smad signaling pathway in a mice model of myocardial infarction.57 It was also revealed that administration of another sesquiterpene compound ameliorated bleomycin-incited lung fibrosis by quelling TGF-β-induced fibroblast to myofibroblast differentiation.58 Here, TGFB1 is linked to myocardial infarction.