In a model of acute myocardial infarction, IL-10 administration significantly suppressed proinflammatory cytokine production, MMP-9 activity, and inflammatory cell infiltration of the myocardium, with a resultant decrease in cardiac fibrosis.7 This resulted in improved left ventricular function and diminished pathological remodeling, including smaller infarct size and less wall thinning. Here, MMP9 is linked to myocardial infarction.