In the early period of MI, MMPs are enrolled predominantly in the process of the myocardial proteins proteolysis and degradation, subsequently MMPs can modulate inflammation and angiogenesis by regulation of ECM and non-ECM substrates (including aggrecan, hyaluronan receptor CD44, complement C1q, connexin 43, fibrinogen, fibronectin, fibroblast growth factor receptor 1 and interleukin-1β), whereas in the later post-MI stages may contribute to excessive fibrosis and adverse remodeling [56,60,61]. This evidence concerns the gene ACAN and myocardial infarction.