On the other hand, at chronic phase after myocardial infarction, in a rat myocardial infarction model, a chymase inhibitor significantly reduced mRNA levels of TGF-β, collagen I, and collagen III, in addition to chymase activity, in the left ventricle, thus improving cardiac dysfunction and fibrosis [28]. Here, CMA1 is linked to myocardial infarction.