The same suppressing impact can be observed in case of the matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) that lead to attenuation of the cardiac inflammation and pathophysiological remodeling, such as replacement of the infarcted area by scar, myocyte hypertrophy, myocyte loss through apoptosis, alterations of endothelial matrix, and endothelial dysfunction [30]. Here, MMP1 is linked to endothelial dysfunction.