Two studies further demonstrated a central role of IL-1β as a ‘pro-fibrotic’ factor after myocardial ischemia: (i) IL-1 receptor type 1 knockout mice showed attenuated myocardial MMP-2 and MMP-3 expression and decreased fibrotic remodeling [30], and (ii) administration of a IL-1 receptor antagonist ameliorated remodeling processes in the infarcted myocardium [31]. This evidence concerns the gene MMP3 and myocardial ischemia.