This conclusion was supported by several experimental results: (1) In an MI mouse model with increased MIAT, levels of TGF-β (transforming growth factor β), an important cytokine that promotes fibrosis, also increased dramatically; (2) MIAT acted as a sponge on miRNAs with anti-fibrotic function, such as miRNA-24, miR-29, miR-30, and miR-133, in the infarcted rat hearts [43]; (3) when performing knockdown MIAT by siRNA or lentiviral, cardiac function was improved, and post-MI cardiac fibrosis was also reduced. This evidence concerns the gene TGFB1 and myocardial infarction.