This modulation of macrophage activity also influences resident cardiac fibrosis, leading to diminished IL-18 expression in fibroblasts, impaired phosphorylation of SMAD2/3 in cardiac fibroblasts, decreased collagen synthesis, and ultimately, the preservation of long-term cardiac function post-myocardial infarction [24]. This evidence concerns the gene SMAD2 and myocardial infarction.