Downstream pathways of TGF-β signaling including p38 mitogen-activated protein kinase (p38), extracellular signal-regulated kinase (ERK1⁄2), c-Jun N-terminal kinases (JNK) and matrix metalloproteinase-2 (MMP-2) was found to be significantly involved in cardiomyocyte injury, repair and remodeling and their pharmacological modulation have yielded significant outcomes in pre-clinical and clinical settings of various cardiovascular diseases including dilated cardiomyopathy, hypertrophy and myocardial infarction [8,9]. This evidence concerns the gene MMP2 and myocardial infarction.