He et al. [53] found that the overexpression of miR-155 in acute myocardial infarction (AMI) induced cardiac fibrosis by directly targeting the Tp53inp1 gene and inhibiting its expression, while downregulated Tp53inp1 dramatically promoted the mRNA and protein expression levels of collagen I/III and increased the expression level of α-SMA in cardiac fibroblasts. This evidence concerns the gene ACTA1 and acute myocardial infarction.