Supporting findings were observed in a mouse model of myocardial infarction, where TIMP-2-deficient mice exhibit increased monocyte/macrophage infiltration alongside heightened MMP-14 expression and activity, promoting adverse disease progression compared with wild-type controls.48 Also, the observation that increased elastin fragmentation alongside macrophage infiltration was more evident in atherosclerotic plaques of TIMP-2-deficient mice, implies a protective role for TIMP-2 in the pathogenesis of aortic aneurysms. This evidence concerns the gene ELN and myocardial infarction.